Gastrointestinal and endocrine disorders

Script to gastro-intestinal and metabolic diseases

based on the "basic textbook of Internal Medicine" (4th edition, Elsevier, 2008)
Sebastian Kuepper
skuepper@uni-muenster.de
Contents
Gastroenterology three reflux disease ..........................................
..... .................................................. ......................
4 gastritis .......................... .........................................
......... .................................................. gastroduodenal ulce
r disease .......................................... ..... 5 ...................
............................... .6 Malassimilationssyndrom .....................
.......................... .................................................. ..
..... 7 colorectal cancer ........................................ .............
..................................... ................... 8 Crohn's disease and
ulcerative colitis ........................ ....................................
.............. Hepatitis ........................ 9 ........................ ...
............................................... ................................
.................. .... 10 liver cirrhosis .....................................
....... .................................................. cholecystolithiasis .
......................... 11 ...................... ............................
...................... ......................................... 12 ....... panc
reatitis .................................................. ....................
.............................. Endocrinology 14 ................ 13 ............
.................. hyperthyroidism .............................................
..... ....................................... 15 ......... hypothyroidism ......
............................................ ...................................
............... ........... .................................... 16 Diabetes mel
litus .................................................. .......................
..... 17 .................... hyperparathyroidism ..............................
.................... literature ................................. 19 20
2
GASTROENTEROLOGY
Signs and symptoms of gastrointestinal disorders
Dysphagia: subjective swallowing disorder (on solid food: mostly mechanical obst
ruction, even in liquid: more neuromuscular). Causes: Esophageal Ca., Peptic str
ictures in reflux, scleroderma, goiter, Zenker's diverticulum. Heartburn: a burn
ing retrosternal pain, often accompanied by acid regurgitation. Dyspepsia: nonsp
ecific upper abdominal discomfort associated with food intake. Causes: reflux, e
sophageal motility disorder, ulcer, gastritis, gastric Ca., Pregnancy, gallstone
s, delayed gastric emptying but functional in 50%!
Indications for further investigation: warning signs (weight loss, performance b
uckling, dysphagia), progression, spec. etiologic information (eg, heartburn), o
lder patients (excluding tumor), longer than 1 month-long refractory symptoms.
Nausea and vomiting: vagal stimulation (Hohlorgandehnung, peritonitis, mucosal i
rritation, nephrogenic / pancreatic / hepatic / biliary afferents), Area-postrem
a-triggering (toxins, opioids, cytotoxic drugs, "pregnancy hormone"), CNS-mediat
ed (intracranial pressure, vestibular stimulation , migraine, meningitis, severe
pain psychogenic). Diarrhoea: osmotically (laxatives, lactose, sorbitol / xylit
ol chewing gum from), secretory (rotavirus bact. Toxin from S. aureus, C. perfri
ngens or V. cholerae, endocrine tumors, fat and bile acids), inflammation (mucos
al irritation at enteritis), motilitätsbedingt psychogenic (, hyperthyroidism, a
fter vagotomy). Constipation: Chronic habit (low-fiber diet, low fluid), organic
bowel disease with obstruction (strictures in IBD, stenosis in carcinoma), gang
lionic motility (Hirschsprung), anal (pain-Defäkationsunterdrückung, eg anal fis
sure). Blood in the stool: at macroscopic melena (tarry) and Hämatochelazie (fre
sh bleeding) and microscopic (occult). Causes: epistaxis, esophagitis, gastritis
, ulcer, Crohn's disease, enteritis, intestinal polyps, NSAIDs, anticoagulants,
and cancer. Abdominal pain is different, "visceral" (abdominal viscera can be tr
ansferred to Headsche zones) and "somatic" pain (parietal peritoneum, act quickl
y!). visceral pain, dull, painful, gnawing, wavy, convulsive or colicky poorly l
ocalized, often median line, projection attempts in other parts of the body the
patient by position change mitigation to provide output of entrails, elongation
of hollow organs, inflammation, visceral hull somatic pain sharp, burning, conti
nuous increasing duration of pain well localized (the patient can draufzeigen fi
nger) Pat takes a posture, not moving breathing, flat output from the parietal p
eritoneum and Mesenterialwurzeln
e.g. Biliary colic,€Constipation, liver capsule pain strain
A hollow organ perforation, peritonitis, bleeding into the abdominal cavity
Acute Abdomen
Acute situation in the abdominal area: acute pain, guarding, decompensation. Cen
tral question: OP indexed? Interdisciplinary diagnostics!
Causes: appendicitis (55%), gallbladder (15%), mech. Ileus (10%), peritonitis (5
%), pancreatitis (5%), more rarely, diverticulitis, renal colic, gynecological E
rkr., Testicular torsion, intestinal ischemia, Organruptur, Extraabdominal (hear
t attack, pneumonia, porphyria).
3
Reflux disease
General reflux of stomach contents (often stomach acid, rare alkali Galle-/Pankr
eassekret) in the esophagus with mucosal irritation. Symptom: heartburn. Heartbu
rn Clinic (mostly postprandial or lying), epigastric pain or restrosternale, Reg
urgation, acid regurgitation. In 10% inflamed mucosa (reflux esophagitis). Compl
ications: peptic stenosis (dysphagia for solid food), Barrett's esophagus (metap
lasia: shattered plates is replaced by columnar epithelium, increased ulcer-and
cancer risk), asthma (chronic stimulation of the vagus). Hoarseness.
10 rule: 10% with reflux esophagitis have, 10% with esophagitis develop Barrett,
10% with Barrett's develop cancer.
Etiology and pathogenesis Inadequate resting pressure of the lower esophageal sp
hincter (eg, scleroderma), prolonged relaxation phase, decrease of peristaltic n
ightly cleaning, hiatal hernia (in 90% of severe erosive esophagitis-Pat.).
Risk factors: obesity, sedentary activity, physical activity, coffee, alcohol, p
regnancy, medications (anticholinergics, theophylline, nitro, opiates).
Diagnostic pH monitoring (pH if pathol. while 7% of the time under 4), manometry
(appreciation of Kardiakompetenz, eg for surgical planning), endoscopy (for sta
ging).
Stages of esophagitis: I-IV (single erythematous erosions in mucous membranes, c
onfluent lesions, circular erosive lesions, ulcers / strictures / Barrett).
Therapy
General measures: weight loss, avoidance of nocturnal meals, healthy diet, diges
tive stroll. Acid reduction: antacids, H2 blockers, proton pump inhibitors (eg o
meprazole, best and fastest results). OP (at Therapieresitenz or severe esophagi
tis): hiatal, Fundopexie or fundoplication.
4
GASTRITIS
General gastritis. Classification by cause (A: autoimmune; B: bacteria, eg H. py
lori, C: chemical, such as NSAIDs), histology (non-erosive = A + B vs. Erosive =
C) and course (acute vs.. Chronic). Clinic
●
erosive gastritis: usually asymptomatic. Possibly. Aversion to food, epigastric
discomfort, dyspepsia. If bleeding: coffee-ground vomiting. In Ggs. to ulcer ble
eding usually no serious bleeding. non-erosive gastritis: autoimmune gastritis i
s asymptomatic, symptoms of pernicious anemia (lack of intrinsic factor, thereby
Vit B12 deficiency), in Helicobacter: dyspepsia (acute), then usually asymptoma
tic. "Real" symptoms until complications (peptic ulcer disease, malignant degene
ration).
●
Etiology and Pathogenesis
●
erosive gastritis: tissue defect to only lamina propria to the exclusion of the
muscularis mucosae (in contrast to the ulcer). Most exogenous (alcohol, NSAIDs),
besides stress gastritis in Intensivpat., Portal hypertension, radiation. Chron
ic erosive gastritis corresponds to type C gastritis. non-erosive gastritis: (a)
autoimmune ("corpus gastritis") with autoantibodies to parietal cells, in 50% i
n addition to intrinsic factor. In the long term reduction of principal cells (a
trophic glands). Possibly. Association of Hashimoto, Addison. (B) bacteria ("ant
ral gastritis") with Helicobacter pylori infection.
●
Diagnostic gastroscopy with biopsy. HP-proof means of urease test (piece of tiss
ue is placed in medium, Helicobacter consumed urea, medium changes color), 13CHa
rnstoff breath test (split orally recorded urea only in the presence of Helicoba
cter detectable then exhaled 13CO2), histology (HE staining) or cultural culturi
ng (consuming, expensive and rarely used). Therapy
● ●
Type A (autoimmune): no specific therapy, it is treated the pernicious anemia. A
nnual follow-up because of cancer risk. Type B (bacterial): Hp eradication alway
s with complication (ulcer, lymphoma), giant folds gastritis (Menetrier's diseas
e), NSAID-taking or erosions (rare).
In asymptomatic patients without risk factors and complications is the Helicobac
ter detection per se is not an absolute indication for eradication is due to the
increased Karzinom-/Lymphomrisikos but often recommended.
●
Type C (chemical, erosive): bleeding prophylaxis in Risikopat. (Sucralfate, H2Bl
ocker), hemorrhage treatment (sucralfate with PPI, endoscopic hemostasis in diff
use bleeding is not possible), discontinue NSAID if possible, not drinking alcoh
ol.
5
Peptic
Peptic ulcer peptic ulcer disease
General Benign mucosal ulcers with circumscribed loss of substance, at least unt
il reaching the muscularis mucosae in (as opposed to erosion). Differentiate acu
te ulcers (erosive gastritis, stress factors, such as OP combustion) and chronic
recurrent ulcer (gastroduodenal ulcer disease =).
Gastric ulcer: v.a. lesser curvature (immediately distal to the säureprod. Korpu
smukosa), atypical location (eg, greater curvature) is karzinomverdächtig. Duode
nal ulcer: duodenal bulb almost always, in Zollinger-Ellison syndrome and distal
.
Clinic
Epigastric pain: gnawing, dull, hungerartig, rhythmic (intensity fluctuates with
time of day / food intake), periodic (symptom change with symptomatic periods).
Furthermore, dyspepsia, nausea, food intolerance. asymptomatic in 20%. Clinical
ly, however, not diagnosed because symptoms nonspecific.
Etiology and pathogenesis of Helicobacter pylori (4-fold increased risk) and NSA
IDs (10% suffer ulcer, of which 10% with a complication, of which 10% fatal), ac
ute physical stress, hypersecretion (gastrinoma). Imbalance between Protektiva (
mucus, blood flow, motility, prostaglandins) and Aggressiva (acid, pepsin, drugs
such as NSAIDs and glucocorticoids). Obligatory: acid. Diagnostic endoscopy wit
h sampling and Hp diagnostics. In 5-10% of ulcerated carcinoma! Therapy
General measures: Nicotine waiver sell, NSAIDs. Acid reduction: proton pump inhi
bitor. Helicobacter pylori eradication: PPI + clarithromycin + metronidazole (It
alian) or PPI + clarithromycin + amoxicillin (French triple therapy) for 7-10 da
ys.
Complications
●
Perforation: a breakthrough in the abdominal cavity, mostly open air (with duode
nal ulcer may also retroperitoneal on the edge of the iliopsoas). Clinical: acut
e abdomen. Diagnosis: Rom-Abdomenübersicht, endoscopy. Treatment: immediate surg
ery. Penetration (= "subdued perforation): Breakthrough in another organ (pancre
as, hepatoduodenal ligament, left lobe of the liver) with no leakage of air. Tre
atment: Surgery. Bleeding: v.a. in NSAID dose. Mortality: 10%. Clinically vomiti
ng blood (hematemesis, coffee grounds), melena (melena). Mostly conservative the
rapy: Endoscopic Submucosal (adrenaline, fibrin glue), while PPI (eg omeprazole)
.
● ●
Classification of ulcer bleeding after Forrest
● ● ●
I: active bleeding: spraying (a) vs. oozing (b). II: currently no bleeding, but
reference to previous history of fresh bleeding: visible vessel (a) vs. Thrombus
Ulcer (b) vs.. Residual blood in the stomach / duodenum (c). III: lesions witho
ut bleeding, bleeding history.
6
MALASSIMILATIONSSYNDROM
General disorders of digestion and absorption in the small intestine. Various ca
uses. Clinic
Chronic diarrhea (fermentation chairs with osmotically active undigested constit
uents, fatty stools, watery in bile acid loss), weight loss, bloating (due to fe
rmentation of indigestible disaccharides, eg lactase deficiency), deficiency (hy
poproteinemia, lack of fat-soluble vitamins, iron deficiency, folate deficiency)
.
Etiology and Pathogenesis
Maldigestion: pancreatic enzymes (chronic pancreatitis, cystic fibrosis), decrea
sed Gallensäurekonz. (Cholestasis, bacterial overgrowth, bile acid loss during r
esection of the term. Ileum). Malabsorption: reduction of resorption (short bowe
l syndrome, Crohn's disease), injury of resorption (infection and bact. Overgrow
th, amyloidosis, celiac disease), intestinal enzyme (lactase deficiency), ischem
ic bowel disease. Lymphatic obstruction: steatorrhea by abnormal chylomicron upt
ake (lymphangiectasia, Whipple, lymphomas).
Diagnosis
Malassimilation: Inspection of the chair, laboratory values (deficiency symptoms
, such as hypoproteinemia, anemia, prolonged bleeding time), stool examination (
stool fat determination, 1-antitrypsin as a marker protein loss). Malabsorptio
n: inflammation, fermentation chairs, pathol. Schilling test (ileal-absorptive:
oral administration of radioactive vitamin B12, vitamin B12 in the measurement o
f the selected 24-hour urine excretion decreased in favor of decreased absorptio
n), pathol. Xylose test (oral xylose in serum and urine decreased speaks for dis
turbed absorption). Maldigestion: fatty stools, normal Schilling and xylose test
. Breath tests: H2 is in the colon in bact. Metabolism of sugars formed.
● ●
Malabsorption in the small intestine: sugar reaches the colon and increases H 2
production, eg with lactase deficiency. Overgrowth in the small intestine: H2 pr
oduction increases immediately, because sugar is already verstoffwechst in the s
mall intestine, without having to get into the colon.
Diseases
●
Celiac disease (gluten enteropathy): Autoimmune disease with hypersensitivity to
gluten (wheat, barley, rye, oats). Diagnosis: Small intestine biopsy (zottenlos
e mucosa). Therapy: elimination diet. M. Whipple: Infection with Tropheryma whip
plei.€Clinic: steatorrhea, abdominal pain, edema by protein loss, arthritis, myo
carditis. Diagnosis: Small intestine biopsy. Therapy: intravenous antibiotic the
rapy, followed for 1 year trimethoprim / sulfamethoxazole. Bile acid loss: Inter
ruption of the enterohepatic circulation (decreased resorption bact. Overgrowth)
. Clinic: watery diarrhea, psychologists, disorder Fettdigestion. Therapy: low-f
at diet, resins, antibiotic treatment.
●
●
7
Colorectal
CARCINOMA CARCINOMA
General One of the most common malignancies in 25% already metastasized at diagn
osis. Almost always adenocarcinoma, benign adenoma often proceeding. Hematogenou
s metastasis in the liver and lung (), lymphatic para-aortic, inguinal and iliac
LKS (). Infiltration of the bladder, ureter, prostate, uterus and ovaries possi
ble (continuous growth). Clinic fatigue, buckling performance, due to lack of tu
mor anemia. GI symptoms until late, and depending on the location: Melena and oc
cult blood loss (prox. colon), change in bowel habits, diarrhea and hematochezia
paradoxical (dist. colon).
Location: rectum 60%, 20% Sigma, 10% caecum / colon ascend., 10% Rest of the col
on.
Etiology and Pathogenesis
Risk factors: age, colorectal adenoma, pos. Family history (2x greater risk), ul
cerative colitis (5x) increases, family Adenopolyposis coli (FAP): 100% degenera
tion.
Genetically adenoma-carcinoma sequence for two special anchored responsible:
●
Polyposis syndrome: juvenile polyposis (hamartomas in 10% malignancies), PeutzJe
ghers (hamartomas, in 3% malignancies), FAP (in 100% malignancy), Gardner (= FAP
with concurrent Knochen-/Weichteiltumoren). Lynch syndrome (HNPCC, hereditary n
onpolyposis colon Ca.): This is the most proximal right colon, by 45 Year of lif
e. Amsterdam criteria: at least three relatives affected, including a first Grad
es used excluded disease in at least two successive generations, at least one <5
0 years, FAP.
●
Diagnosis
Investigation: possibly palpable mass in the lower abdomen, rectal examination,
fecal occult blood. Colonoscopy with biopsy: method of choice. Staging: sonograp
hy (liver!), CT. Labor: Tumor markers CEA and CA 19-9 (follow-up, not for primar
y diagnosis!).
UICC IA Dukes B1 T 1 2 N 0 M 0 0 0 5-year survival> 85% 90% Explanation tumor li
mited to mucosa or submucosa invasion of muscularis
II III IV
B2 C D
3 each 4 each each
0 0 1 2 each
0 0 0 0 1
70-80% 35-65% <5%
Infiltration of the subserosa infiltrated visc. Peritoneum / organs affected lym
ph nodes metastases
(UICC = International Union Against Cancer, 5-year survival = 5-year survival ra
te in USA)
Therapy
OR (as advanced stages) benefit. Objective: Radical tumor resection with a safet
y distance of 5cm, eliminating local LKS. Kontinenzerhaltend if at least 2 cm di
stance remaining to the anus. Ileostomy: aggressive thinner chair, expensive car
e, the patient significantly reduced. Colostomy: rather solid stool, easier main
tenance. Radiotherapy / chemotherapy of minor importance. Indications for chemot
herapy: UICC III (eg, adjuvant 5-fluorouracil, folinic acid and oxaliplatin afte
r FOLFOX regimen).
8
Crohn's Disease
General
AND
Ulcerative Colitis
Colitis
Nonspecific, chronic inflammatory bowel disease (IBD) with loss of mucosal integ
rity, decreased resorption and increased secretion and excretion. Differences in
appearance and distribution pattern. Clinic Because inflammatory changes and th
eir effects on the intestinal wall.
Crohn's disease:
● ● ● ● ● ●
General symptoms: weight loss, anorexia, weakness. Abdominal pain: diffuse, cram
ping later, depending on location of infestation. Diarrhea (if colon affected):
occasional admixture of blood. Obstruction (by entz. / fibrotic bowel wall thick
ening): subileus-weight. Fistulae, abscesses, perianal changes (fissures, fistul
as, abscesses). extraintestinal manifestations cholangitis, erythema nodosum, ar
thritis. Diarrhea: bloody, slimy (and night), 10-20 per day, possibly tenesmus.
no perianal changes, rare extraintestinal manifestations.
Ulcerative colitis:
● ●
Etiology and pathogenesis remains unclear. Genetic, immunologic and environmenta
l factors.
Crohn's entire GI tract can be affected: preferred ileum, colon (omitted rectum)
segmental or diffuse distribution of discontinuous propagation ("skip lesions")
affect all layers of the wall (transmural) ulcerative colitis to the colon boun
ded (rectum always involved) diffuse distribution continuous propagation limited
to mucosa
At most slightly increased risk of cancer diagnosis
Cancer risk increases
Clinical, laboratory and endoscopy (with histology). Unambiguous assignment is n
ot always poss.
● ●
Crohn's disease: Lab: increased Entz.parameter, ASCA pos. (70%), KM-ray image: c
razy paving; Endoscopy: "skip lesions and mouth ulcers. Ulcerative colitis: Lab:
increased Entz.parameters, anemia, pANCA pos. (70%), KM-X-ray: mucosal ulcerati
ons, pseudo polyps, Haustrenschwund (inner tube), endoscopy Rektumbefall obbliga
to.
Therapy
acute phase: diet (possibly parenteral nutrition), glucocorticoids, azathioprine
, cyclosporine, methotrexate, in Crohn's disease: infliximab (monoclonal TNF-ant
ibody). Term therapy: 5-amino-salicylates (5-ASA).
In ulcerative colitis as a last resort: colectomy (curative). Crohn's disease: n
o cure.
9
HEPATITIS
General Numerous causes (viruses, toxins, drugs) can lead to liver cell necrosis
with infiltration of the tissue with inflammatory cells. Extremely variable cou
rse. Classification: acute vs. Chronic (> 6 months) or cause (infectious, toxic,
autoimmune, hereditary). Clinic of hepatitis virus
Prodromal stage (days to weeks) with nausea, vomiting, anorexia, fever, upper ab
dominal pain, arthralgia, disturbed taste, cigarette aversion. Organ manifestati
on (up to 8 weeks): liver tenderness, jaundice, itching. Forms:
● ●
anicteric (especially Hep. C): in 50% of hepatitis, often completely asymptomati
c course. cholestatic (especially Hep. A and B) in 5% of patients Stuhlentfärbun
g, increased cholestasis (bilirubin, -GT and AP), AZ-significant reduction. bri
lliant (especially Hep. B, pregnant women with Hep. E): progressive liver failur
e: hepatic encephalopathy, cerebral edema, hypoglycemia, GI bleeding, respective
ly. Insuff., Infection tendency. Histologically: bridging necrosis. Transplantat
ion indexed! Chronic (Hep B, C and D):> 6 months existing transaminases increase
. Clinically reduced performance, fatigue, intermittent anorexia. Diarrhea.
●
●
Laboratory findings
Transaminases (usually 15-fold increase), GOT / GPT <1 (De Ritis ratio), bilirub
in increased most strongly (directly and indirectly in equal proportion) in chol
estatic course: in addition -GT and AP increased. Serology: detection of antibo
dies against certain hepatitis viruses or their components. In addition, determi
ning autoantibodies to exclude autoimmune hepatitis (ANA, AMA, LMA, LKM, SLA).
Therapy 40% of clinically apparent viral hepatitis need treatment: abstinence fr
om alcohol until normalization of liver function tests, no discontinuation of ur
gently needed medications. Glucocorticoids indicated, as favoring a chron. Cours
e! Forms of acute viral hepatitis
Hepatitis A: fecal-oral, a typical tourist disease, asymptomatic in 50%. Diagnos
is: Anti-HAV IgM-AK detectable after 14d. Therapy: general hygiene measures. Pre
diction: in 99% healed within three months. Hepatitis B: common viral hepatitis,
transmission perinatally, parenterally and sexually. Diagnosis: Anti-HBc-IgM Ab
and HBs Ag is proof of acute infection. Anti-HBe and anti-HBs AK remain lifelon
g. Treatment: none. Forecast: 90% inconsequential healing, 10% of asymptomatic c
arrier state, 1% fulminant chronic (cancer risk), 1%. Hepatitis C: Transmission
parenterally and sexually, usually asymptomatic course. Diagnosis: anti-HCV-AK,
HCV-RNA detection. Therapy: early 24-week interferon therapy can prevent chronic
in almost 100%. Forecast: untreated chronic course in 80%, 20% in liver cirrh
osis with increased cancer risk. Hepatitis D: only when co-infection with hepati
tis B pathogen. Diagnosis: anti-HDV-IgM-AK.
10
Cirrhosis
General irreversible end-stage fibrotic scarring with destruction of the lobules
and vascular structures, inflammatory fibrosis and Regeneratknotenbildung. Clin
ical symptoms of portal hypertension (see below) and hepatocellular dysfunction:
● ● ● ● ●
General symptoms: fatigue, reduced performance, weight loss. Skin: jaundice, spi
der nevi, white nails, Lackzunge, skin atrophy, palmar erythema, caput medusae,
petechiae, abdominal baldness, gynecomastia. Foetor hepaticus. Edema: by hypoalb
uminemia. hepatic encephalopathy: grobschlägiges hands trembling ("flapping trem
or"), consciousness disturbance, apraxia, apathy, coma.
Etiology and pathogenesis of 50% alcohol, 25% of chronic viral hepatitis (B, C,
D), other: autoimmune hepatitis, drug-toxic liver damage, biliary cirrhosis (PBC
, Caroli's syndrome), M. Wilson, hemochromatosis, Budd-Chiari syndrome (hepatic
vein thrombosis). Alcohol: intermediate fatty liver and fatty liver hepatitis, t
hen small nodular cirrhosis. For other causes: postnekrotische macronodular cirr
hosis with nodes. Diagnosis
Lab: Liver disease (decreased: CHE, vitamin K-dependent coagulation factors, Pro
thrombin time, AT-III, proteins C and S, albumin, increased: GOT, GPT,-GT , Bil
i, ammonia). Sonography: non-homogeneous pattern, rounded liver edge, irregular
surface. Biopsy indicated: only in exceptional cases, since therapeutic result o
n clinical examination.
Therapy
General measures: avoid noxious substances, protein and calorie diet, folic acid
. If necessary. specific therapy,€if not too advanced cirrhotic remodeling (blee
ding in hemochromatosis, Immunsuppress. in autoimmune hepatitis, virus eliminati
on). If necessary. Liver transplantation. Forecast: depending on Child-Pugh scor
e (from albumin, ascites, bilirubin, Quick and encephalopathy formed a score tha
t correlates with prognosis).
Complications
Ascites: an excellent distention, increased abdominal girth. Risk of spontaneous
bacterial peritonitis. Washing out too quickly: hepatorenal syndrome. Portal hy
pertension: gastric fundus and esophageal varices, portal gastropathy. Therapy:
propranolol, nitrates (reduction of portal pressure), Terlipressin in bleeding,
ligation / sclerotherapy after hemorrhage, transjugular intrahepatic porto-syste
mic shunt (TIPS) allows connection between the hepatic and portal veins. Hepat.
Neurotoxic encephalopathy: through enrichment. Substances (e.g. ammonia).
11
Cholecystolithiasis
General prevalence to 15%, of which 1% / year operating restitutor symptoms, app
roximately 75% asymptomatic. Clinic 75% asymptomatic ("silent stones"), nonspeci
fic upper abdominal discomfort (bloating, flatulence, nausea, vomiting), acute b
iliary colic (usually stone passage in the cystic duct): plötzl. beginning, an i
ncrease of hours, broadcasting right shoulder. When thinking of jaundice in the
common bile duct stone. Etiology and pathogenesis Increased cholesterol synthesi
s or bile acid loss. Risk factors ("female, fat, forty, fertile, family"): high-
fat diet, obesity, female hormones, pregnancy, family history. Diagnosis
History: character of the pain, previous history of colic, decolorized chair. In
vestigation: bulging of the abdominal wall, careful palpation, jaundice, Murphy'
s sign. Labor: CRP, cholestasis parameters ( -GT, alkal. phosphatase, bilirubin)
increased in speed shutter, lipase and amylase increases associated with pancre
atitis. Sonography: Stones (posterior acoustic shadow), inflammation (acute: thr
ee layers, chronic: thickening of the wall), duct dilatation as an indication of
stones in the passage.
Therapy With simultaneous jaundice (bile duct = cap): rapid ERCP with papillotom
y.
● ● ●
asymptomatic: no treatment required. Colic: pain (spasmolysis with scopolamine,
analgesia with metamizol, alternatively pethidine). Except not use pethidine mor
phine (spasmogen!). symptom-free interval: Stone Removal (1st choice: laparoscop
ic surgery; aka extracorporeal shock wave therapy).
In acute cholecystitis: stabilization of the patient (fasting, Schmerzther., Ant
ibiotics), then the OR. In perforation surgery within the next few hours! Compli
cations
●
acute cholecystitis with empyema, upper abdominal pain, severe malaise, fever, c
hills, leukocytosis. Clinical: Murphy's sign (deep inspiration is terminated by
pain when palpating finger triggers gallbladder below the right costal margin).
Ultrasound: three layers of the GB wall. . Chron Cholecystitis: non-specific sym
ptoms (abdominal fullness, nausea), pressure in the upper abdomen, pain on deep
palpation. Ultrasound: wall thickened. Perforation: biliary peritonitis (high mo
rtality rate!), Possibly gallstone (when migrating through the stone in the duod
enum or colon). Rom-abdomen: bile ducts. Porcelain GB: rock hard calcium deposit
s with GB (increased cancer risk). acute biliary pancreatitis: with stone passag
e until closure of the papilla and D. hepaticopancreaticus.
● ● ● ●
12
Pancreatitis
Acute pancreatitis after switching off the trigger rule to expect healing. Sympt
om: abdominal pain, possibly radiating to the back, elastic waist (elastic waist
voltage).
Clinic
Abrupt onset, severe abdominal pain, often radiating a belt in the back, nausea,
vomiting. Typical: rubber belly. Characters: petechial hemorrhage, target lesio
ns (Cullen), or in the flanks (Grey-Turner). In advanced disease: somatic pain (
well localized, parietal peritoneum affected).
Division
● ●
Easy: moderate pain, enzyme rise, low Parenchymschäden (edema). Expert: local (n
ecrosis, abscess, pseudocyst) or organ complications (ARDS, disseminated intrava
scular coagulation, acute renal failure).
Complications: pseudocyst, bacterial superinfection of necrosis, paralytic ileus
, hyperglycemia, hypocalcemia (Ca2 +-binding in fat necrosis), sepsis.
Causes
Biliary and binge-drinking by far the most! Rare: medications (including diureti
cs, steroids, interferon), post-ERCP, autoimmune, primary hyperparathyroidism.
Laboratory diagnosis: Lipase (at least 10-fold increase) and -amylase (4x), CRP
, leukocytosis. In severe cases: LDH increased, hypocalcemia, lactic acidosis. I
n biliary etiology: Cholestasis. Sonography: edema, ascites, necrosis, pseudocys
ts, bile (away) stones, possibly CT. Therapy
ICU! In V.a.€Biliary etiology: ERC (without pancreatic duct display), possibly w
ith papillotomy. Treatment goals:
● ● ●
Pancreas are quietly leave food and liquid, gastric tubes, PPI administration. P
ain: Fighting procaine Perfusor, possibly in addition metamizol, pethidine. If n
ecessary. Epidural catheter. Complications: Avoid parenteral fluid (5l/24h), sys
temic antibiotics, heparin. Surgical indication (cautious, because high mortalit
y rate!): Not under control, intensive care complications (infected necrosis, pa
ncreatic pseudocyst).
Chronic pancreatitis with inflammatory Progressive irreversible damage and incre
ased cancer risk. Clinically relapse. Upper abdominal pain, nausea, malabsorptio
n, fatty stools, diabetes mell. Reasons: in 2 / 3 alcohol, pancreatic duct obstr
uction (tumor, inflammation), hereditary, and rare cystic fibrosis, prim. Hyperp
arathyroidism, hyperlipidemia. Diagnosis: ultrasound, ERCP, CT. itis distinction
between tumor and not always possible. Therapy: abstinence from alcohol, elimin
ate runoff barriers, symptomatic treatment: acute episodes such as acute pancrea
titis, pain treatment, exocrine / endocrine insufficiency.
13
ENDOCRINOLOGY
Classification of endocrine disorders
● ● ●
Primary: disruption of the gland (= peripheral hormone). Secondary: fault on pit
uitary level (= glandotropes hormone). Tertiary: fault on hypothalamic-level (=
releasing).
A disturbance is an autonomous, decoupled from the feedback inhibition of secret
ion.
Signs and symptoms of hormonal imbalances
● ● ● ●
General: fatigue, weakness, depression, appetite / thirst, and thermal sensation
changes, anxiety, palpitations, tremor. Changes in physique: height, weight. Sk
in pigmentation, dryness, sweating, hair loss, hirsutism. Sexual organs: libido
/ potency changed, cycle disorder, gynecomastia.
Diagnosis of hormonal disorders
Basal levels due to daily fluctuations and variable protein binding is often dif
ficult to interpret and susceptible. Alternative: provocation test.
● ●
Stimulation test: parent hormone (glandotrop or releasing covers) decreased Sekr
etionskapazität of the gland (hypothyroidism = on). Suppression test: peripheral
hormone suppressed normally glandotropen via feedback inhibition of the secreti
on of the parent or releasing hormone. Lack of suppression: Autonomy or ectopic
tumor (= hyperthyroidism).
To localize the fault: sonography, CT, MRI, scintigraphy.
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Hyperthyroidism
General almost always primary, rarely secondary / tertiary. Severity: latent / s
ubclinical (TSH decreased, normal T3/T4), manifest (T3/T4 increased, most sympto
ms), thyrotoxicosis (life threatening, eg after contrast with existing autonomy:
sinus tachycardia, fever, vomiting, restlessness, delirium, shock , coma). Very
variable clinic. Hypermetabolism (sweating, heat intolerance, weight loss), cat
echolamine sensitivity increased (tachycardia, palpitations, arrhythmia), diarrh
ea, palmar erythema, feinschlägiger finger tremor, restlessness, nervousness (up
to psychosis!). Etiology and Pathogenesis
● ●
functional autonomy: unifocal (= adenoma), multifocal or disseminated. Graves' d
isease: autoantibodies against TSH receptor with receptor-term stimulation. Clin
ically Merseburg triad of goiter, exophthalmos, tachycardia. In addition, thyroi
d eye disease (Mobius, Grafe, Dalrymple-and Stellwag sign) and dermopathy. more
rarely, subacute thyroiditis (de Quervain), Hashimoto's thyroiditis with transie
nt (Hashi-Toxicity), TSH produze. Tumor, ectopic hormone formation (struma ovari
i).
●
Diagnosis basal TSH (if normal, hyperthyroidism excluded if decreased: T measure
3/T4), in Graves' disease: TSH receptor antibodies, often anti-TPO, and Sono-sc
intigraphy. Therapy
● ●
Functional Autonomy: Bridging: thyreostatic, definitely: Surgery, radioiodine. G
raves' disease: antithyroid for 1-2 years, then TSH. If necessary. OP / radioiod
ine.
Antithyroid are thionamides (Favistan, Carbimazole) or perchlorate (Irenat). Thy
rotoxic crisis (ICU!): High dose thyroid antagonists, beta-blockers, glucocortic
oids, acute subtotal Thyreodektomie at Iodkontamination, possibly plasmapheresis
(removal eiweißgebundener hormones). Comments Graves' disease usually speaks we
ll to antithyroid and leads in 40% to permanent remission. In functional autonom
y is preferred OP (before seeking euthyroidism!), In hyperthyroidism iodinduzier
ter immediately OP. Postoperative: possibly hypothyroidism, which are permanentl
y treated with thyroid hormone (Euthyrox) must. After radioiodine therapy, it is
common to hypothyroidism (50% after 20 years). Complications after surgery: N.
relapsing-injury (chronic unilaterally. hoarseness, both sides: vocal cord paral
ysis), hypoparathyroidism with tetany (Ca2 +-control post-operative) in Mitentfe
rnung of the parathyroid glands, hypothyroidism.
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Hypothyroidism
General lack of thyroid hormone in the target organs. The most common cause in a
dults: Hashimoto's thyroiditis. Rare: secondary, rarity: tertiary. Creeping clin
ic. Hypometabolism (cold intolerance, weight gain, apathy), catecholamine sensit
ivity decreased (bradycardia), pasty skin, muscle weakness, diminished reflexes,
constipation, depression. In children: failure to thrive.
Myxedema (subcutaneous mucopolysaccharides): pericardial effusion, bloated body,
edema does not leave any dents (in contrast to cardiac edema). Myxedema coma (e
xtremely rare): hypoventilation, hypothermia, hypotension. Most in-HVL failure.
Etiology and Pathogenesis
● ●
congenital (heterogeneous, eg, thyroid aplasia, Iodverwertungsstörung): Macroglo
ssia, constipation, jaundice neonatorum prolongatus, developmental disabilities,
cretinism. acquired: the final state after all inflammations (especially Hashim
oto, rarely Basedow), iatrogenic (treatment of hyperthyroidism) or excessive iod
ine deficiency, and lithium.
Diagnosis basal TSH (if normal: hypothyroidism excluded if: increase measure T4)
. T3 can be low or normal (through increased conversion). In Hashimoto: AntiTPO
antibodies, occasionally associated with type I diabetes, sprue, myasthenia grav
is. Almost always, life-long substitution therapy with L-thyroxine (Euthyrox). E
xceptions: transient forms such as antithyroid-induced hypothyroidism or thyroid
itis de Quervain's (viral or parainfectious). Objectives: Beschwerdfreiheit, nor
malization of TSH.
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DIABETES
General
MELLITUS
In industrialized countries most common cause of blindness and dialysis. Disturb
ance of glucose, fat and protein metabolism due to insufficient insulin action i
n liver, fat and muscle cells (type I: lack of insulin, Type II: insulin resista
nce, both types) to take. Insulin secretion in adults: 40 IU / day (high to food
, low in hunger).
Secretion:
Basal secretion (Maximum early morning / late afternoon) and pro-secretory facto
rs: -adrenergic stimulation, leucine, mannose (glucose-dependent) and GIP, chol
ecystokinin, secretin, gastrin, lysine, fatty acids, ketone bodies, ACh (vagus),
GLP1 (amplification of the glucose effect on the B-cell).
Inhibition of secretion:
Insulin (negative feedback), 2-adrenergic stimulation, chronically elevated Gl
ukosekonz.
Effect of insulin:
Increase anabolism (glycogen, lipid and protein synthesis), inhibition of catabo
lism (glycolysis, lipolysis, proteolysis, gluconeogenesis) and influx of K +.
Insulin antagonists:
Glucagon, epinephrine, norepinephrine, glucocorticoids, growth hormone. Clinic
● ●
Type I: <40 years, mostly acute hyperglycemia symptoms: polyuria, polydipsia, de
hydration, weight loss, fatigue, immune deficiency (UTI, thrush, itching), coma.
Type II: older patient, usually damages: neuropathy, nephropathy, stroke.
Etiology and Pathogenesis
● ●
Type I (insulin deficiency): autoimmune-mediated destruction of B-cells (trigger
unknown), clinically significantly from 80% cell death, HLA association. Type I
I (insulin resistance): genetic predisposition, no HLA association, overeating,
lack of exercise.
Hyperglycemia leads to tissue damage (microcirculation in type II also macroangi
opathy by atherosclerosis and hypertension). Diagnosis
fasting normal OGTT 2 h value
<110 mg / dl (6.1 mmol / l) <140 mg / dl (7.8 mmol / l) impaired Gluk.toleranz 1
10-126 mg / dL 140-200 mg / dl diabetes> 126 mg / dl (7 , 0 mmol / l)> 200 mg /
dl (11.1 mmol / l) or: casual-BZ> 200 mg / dl with polydipsia, polyuria, and une
xplained weight loss, metabolic syndrome: Type II-Diabetes/gestörte glucose tole
rance / insulin resistance (at least . one of them) + hypertension / obesity / d
yslipidemia / microalbuminuria (at least 2 of them). Always look for Folge-/Begl
eiterkrankungen: renal function (creatinine, U-status), lipid status, fundus is
angiological investigation (PAD), vibratory (neuropathy), thyroid (type I diabet
es associated with autoimmune thyroiditis).
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Therapy
Goals: Avoid long-term damage by the closest possible BZ-setting and consistent
treatment of concomitant diseases (hypertension, dyslipidaemia). Intensified ins
ulin therapy with HbA1C <7% is superior to the standard insulin therapy clearly!
● ● ●
Lifestyle: regular meals, avoid movement, other vascular risks. Metabolic self-r
egulation: BZ-control crucial determining prognosis. Diet: weight loss (type II)
, full balanced mixed diet (no special diabetic diet, but on three main distribu
ted-and three snacks), avoid high glucose index (table sugar), rather, complex c
arbohydrates. BE-need per day: 14 (normal), 28 (hard working), 7-10 (weight loss
). Drugs: Insulin or oral antidiabetic agents.
●
Insulin therapy
Indication: all Type I diabetics, therapy-refractory type II diabetics.
● ●
conventional: 2x daily€Misch-/Verzögerungsinsulin (2 / 3 breakfast, 1 / 3 dinner
). intensified (basal-bolus): 1-2x daily insulin delay, additional short-acting
insulin before meals. Expensive, more frequent self-regulation, training!
Insulin preparations: fast-acting (Lys-Pro insulin, insulin), delay insulin (int
ermediate-and long-acting), mixed insulin (intermediate-plus insulin). "After 40
correct" rule means that if current fuel cell above the target (eg 200 instead
of 120 mg / dl), shall be injected in the region above the target value for each
40 mg / dl glucose 1 IU insulin (here: two IE). Which diabetic insulin per unit
which reacts with BZ-reduction is to be tried individually and needs. So there
are also patients, to correct for either 30 or 50 rule.
Therapy with oral antidiabetic
1st Choice for recruitment of type II diabetes when diet has not helped.
●
Biguanides (eg metformin): delayed glucose absorption (intestine), inhibition of
gluconeogenesis (liver) and increased glucose uptake (muscle cell). Advantages:
no hypoglycemia, no Insulinmast, lowering triglycerides. Disadvantages: GIStöru
ngen, lactic acidosis (before OPs sell!), Blood count changes. Glitazones (such
as Actos): Insulinsensitizer (fat, muscle and liver tissues, so extrapancreatic)
. Cheap endothelial effects and lipid lowering. Sulphonylurea analogues (eg Novo
Norm): glucose-InsulinsekretionsSteigerung, possible combination with metformin.
Sulfonylureas (eg glibenclamide): protracted hypoglycemia in older specimens. M
etab. Syndrome is more likely to increase, so use caution.
● ● ●
Acute complications
Hyperglycemia: hyperosmolar non-ketotic syndrome (mostly Type II), diabetic keto
acidosis (type I). Both are called "diabetic coma", also mixed forms are possibl
e. Hypoglycaemia: e.g. Insulin overdose. Early symptoms of beta-blockers veiled!
Comments patient education (nutrition, BZ-self-measurement, recognize symptoms o
f hypoglycemia, foot care to avoid, risk factors), HbA1C control (depending on t
he laboratory: from 4 to 6.2%) every three months, at every doctor visit walk-ex
amination.
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Hyperparathyroidism
General parathyroid hormone (PTH) is produced in four parathyroid glands (back o
f the thyroid). Function: Prevent Hypocalcaemia (antagonist: Calcitonin). Effect
s: release of Ca2 + and PO43-(skeletal), increasing the Ca2 +-absorption, PO43 -
VitaminD3 excretion and synthesis (kidney). Primary hyperparathyroidism is rela
tively common, in addition to malignancy most common cause of hypercalcemia, usu
ally sporadic, rarely in the context of a multiple endocrine neoplasia (MEN synd
rome). Causes: solitary adenoma (80%), hyperplasia (20%) or parathyroid carcinom
a (<1%).
Clinic
In 50% asymptomatic, often found as part of the routine laboratory (hypercalcaem
ia). Renal and osseous symptoms in the foreground.
● ● ● ● ● ●
Renal: nephrolithiasis, nephrocalcinosis ("stone"). bony: osteopenia, pathologic
al fractures, Maximalform: osteitis fibrosa cystica Generalisata Recklinghausen
("leg"). Gastrointestinal: ulceration due to increased Gastrinproduktion ("Magen
pein"). psychological: psychosis, depression. Neurological: proximal muscle weak
ness, fasciculations. general: polyuria, polydipsia, nausea, constipation, rapid
fatigue.
Diagnosis
Laboratory: serum intact PTH increased, hypercalcemia, elevated alkaline phospha
tase.
Therapy
Only curative option: surgical removal of the affected parathyroid gland (s). Po
stoperative risk of hypocalcemia, so regular laboratory checks. Secondary hyperp
arathyroidism typical complication of chronic renal failure, rarely in malabsorp
tion. Cause: hypocalcemia and / or vitamin D deficiency. Clinic: Bone pain, spon
taneous fractures. (No nephrolithiasis, because no hypercalcaemia!) Diagnosis: i
ntact PTH and alkaline phosphatase increased, normal calcium / low, often hyperp
hosphatemia. Therapy: reduction of phosphate, vitamin-D substitution, possibly P
arathyreodektomie. Objective: Normalization of calcium and phosphate levels, pre
venting extraosseous calcifications. Tertiary hyperparathyroidism autonomous hyp
erfunction of the parathyroid glands in secondary hyperparathyroidism many years
(PTH secretion independent of Ca2 + levels, disturbed neg feedback mechanism).
Most dialysis patients after long-standing renal insufficiency. Absolute Surgica
l Indications!
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LITERATURE
General
● ● ●
Classen M, Diehl V, Kochsiek K et al. (2004): Internal Medicine. 5th Edition. Lo
ndon: Elsevier. Kasper DL, Braunwald E, Fauci AS et al. (2008): Harrison's Princ
iples of Internal Medicine. 17th Edition. New York: McGraw-Hill. Renz H-pads, Kr
autzig S (2008): Basic Textbook of Internal Medicine. 4th Edition. London: Elsev
ier.
Gastroenterology
● ●
Feldman M, Friedman LS,€Brandt LJ (2006): Sleisinger & Fordtran's Gastrointestin
al and Liver Disease. 8th Edition. Philadelphia: Saunders. Yamada T, Alpers DH (
2008): Textbook of Gastroenterology. 5th Edition. Philadelphia: Lippincott Willi
ams & Wilkins.
Endocrinology
●
Kronenberg HM, Melmed S, Polonsky KS et al. (2007): Williams Textbook of Endocri
nology. 11th Edition. Philadelphia: Saunders.
is the current version of this script are available for download at the address
http://www.harvey-semester.de/
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