Morning Report

Friday, 15th December of 2017

5th Team
Identity
 Name: Mrs. A
 Age : 49 Years Old
 Address: Naasir Street No.12, Cawang
 Educational Background : High School
 Status : Married
 Nation : Indonesian/Javanese
 Religion : Moslem
Chief Complain : Diarrhea since 2 days ago.
Physical Examination
 LOC : E4 M6 V5, compos mentis
 BP : 150/90 mmHg
 PR : 106 x/ mnt
 RR : 20 x/mnt
 Temp : 36,40C
General Examination
 Head : normocephali
 Eye :
 conjungtiva anemic -/-
 Sclera icteric -/-
 Neck :
 JVP normal
 Lymphoid undetected
 Thorax :
 I : movement of chest wall symmetric left-right
 Pal : Vocal fremitus symmetric
 Per : Sonor/sonor
 Aus : basic breath sound vesicular ,
 Ronchi -/-, wheezing -/-, heart sound I & II regular, murmur (-) gallop
(-)
Continued…
 Abdomen :
 Ins : stomach looks flat
 Aus : bowel sound 4 times/minutes
 Per : Tympany, percussion pain (-)
 Pal : supple, tenderness in epigastric area
 Ext : peripheral warm, capillary refill <2 ‘’ edema (-,-/-,-)
Therapy
 IVFD : III Ringer Laktat/ 24 hour
 mm:
 Ciprofloxacin 2 x 200mg (IV) Omeprazole 1 x 40mg (IV)
 Newdiatabs 1 x2 tab prn (PO)
 Donperidone 3 x10mg (PO)
 Metformin 3 x 500mg (PO)
Planning
 Pro Hospitalized
 ECG
 Diet : soft food and low carbohydrate
 Lab : H2TL, GDS, Electrolyte
References
Acute Gastroenteritis
 Acute Abdomen

Intraluminal Extraluminal Gastrointestin Paralytic Blunt Miscellaneous

Obstruction Obstruction al Ileus Trauma
Disease

Foreign Body Hernia Appendicitis Sepsis Accident Lead poisoning

Bezoar Intussusceptio Crohn disease Pneumonia Battered child Sickle cell
Fecalith n Ulcerative Pyelonephritis syndrome disease
Gallstone Volvulus colitis Peritonitis Familial
Parasites Duplication Vasculitis Pancreatitis Mediterranean
Stenosis Peptic ulcer fever
Cystic fibrosis Cholecystitis
Tumor disease Porphyria
Tumor Renal stones
Mesenteric cyst Meckel’s DKA
Fecaloma Gallstones
SMA syndrome AGE Addisonian
PID crisis
Pyloric stenosis Lymphadenitis Testicular
torsion
Ovarian Torsion
Approach
 History
 Symptoms
 Nausea, emesis, retching
 Abdominal pain
 Bowel movements
 Timing
 Age
 Onset
 Relation to feeds
 Focus of infection, other affected individuals
Approach
 Physical examination
 Temperature, heart rate, blood pressure, pain
 Abdominal examination
 Auscultation before palpation
 Palpation
 Masses
 Tenderness
 Auscultation for bowel sounds
Approach
 Objectives
 Assess the degree of dehydration
 Prevent spread of the enteropathogen
 Selectively determine etiology and provide specific therapy
Dehydration
 Mild (3-5%)
 Normal or increased pulse
 Decreased urine output
 Thirsty
 Normal physical exam
Dehydration
 Moderate (7-10%)
 Tachycardia
 Little/no urine output
 Irritable/lethargic
 Sunken eyes/fontanelle
 Decreased tears
 Dry mucous membranes
 Skin- tenting, delayed cap refill, cool, pale
Dehydration
 Severe (10-15%)
 Rapid, weak pulse
 Decreased blood pressure
 No urine output
 Very sunken eyes/fontanelle
 No tears
 Parched mucous membranes
 Skin- tenting, delayed cap refill, cold, mottled
Dehydration
 Treatment
 Calculate deficits
 Water: % dehydration x weight
 Sodium: water deficit x 80 mEq/L
 Potassium: water deficit x 30 mEq/L
 Treat mild-moderate dehydration with oral rehydration
solutions
 May treat severe dehydration with intravenous fluids
 Hyponatremic v. isotonic v. hypernatremic
Etiology
 Enteropathogens
 Non-inflammatory vs. inflammatory diarrhea
 Non-inflammatory
 Enterotoxin production
 Destruction of villi
 Adherence to GI tract
 Inflammatory
 Intestinal invasion
 Cytotoxins
Etiology
 Chronic diarrhea
 Giardia lamblia
 Cryptosporidium parvum
 Escherichia coli: enteroaggregative, enteropathogenic
 Immunocompromised host
 Non-infectious causes: anatomic, malabsorption,
endocrinopathies, neoplasia
Etiology
 Bacterial
 Inflammatory diarrhea
 Aeromonas
 Campylobacter jejuni
 Clostridium dificile
 E. coli: enteroinvasive, O157:H7
 Plesiomonas shigelloides
 Salmonella
 Shigella
 Vibrio parahaemolyticus
 Yersinia enterocolitica
Etiology
 Bacterial
 Non-inflammatory
 E. coli: enteropathogenic, enterotoxigenic
 Vibrio cholerae
 Viral
 Rotavirus
 Enteric adenovirus
 Astroviruus
 Calcivirus
 Norwalk
 CMV
 HSV
Etiology
 Parasites
 Giardia lamblida
 Entamoeba histolytica
 Strongyloides stercoralis
 Balantidium coli
 Cryptosporidium parvum
 Cyclospora cayetanensis
 Isospora belli
Diagnosis
 History
 Stool examination
 Mucus
 Blood
 Leukocytes
 Stool culture
Diagnosis
 Examination for ova and parasites
 Recent travel to an endemic area
 Stool cultures negative for other enteropathogens
 Diarrhea persists for more than 1 week
 Part of an outbreak
 Immunocompromised
 May require examination of more than one specimen
Antimicrobial therapy
 Aeromonas
 TMP/SMZ
 Dysentery-like illness, prolonged diarrhea
 Campylobacter
 Erythromycin, azithromycin
 Clostridium dificile
 Metronidazole, vancomycin
 E. coli
 TMP/SMZ
Antimicrobial therapy
 Salmonella
 Cefotaxime, ceftriaxone, ampicillin, TMP/SMZ
 Infants < 3 months
 Typhoid fever
 Bacteremia
 Dissemination with localized suppuration
 Shigella
 Ampicillin, ciprofloxacin, ofloxacin, ceftriaxone
 Vibrio cholerae
 Doxycycline, tetracycline
Therapy
 Antidiarrheal medication
 Alter intestinal motility
 Alter adsorption
 Alter intestinal flora
 Alter fluid/electrolyte secretion
 Antidiarrheal medication generally not recommended
 Minimal benefit
 Potential for side effects
Prevention
 Contact precautions
 Education
 Mode of acquisition
 Methods to decrease transmission
 Exclusion from day care until diarrhea subsides
 Surveillance
 Salmonella typhi vaccine
 Type 2 Diabetes Mellitus

Aetiology, Pathogenesis, History, and Treatment

The Diabetes Mellitus epidemic
 Estimated 180 million people in the world have
DM. That’s roughly 6% of the world population.
 These numbers are estimated to double by 2030.
 Healthcare costs approaching 92 billion a year for
the U.S.
What is Diabetes Mellitus?
 A metabolic disorder that results when the body
is unable to maintain adequate insulin secretion to
prevent hyperglycemia.
 Disease classification:
Type 1 or Type 2
 90% of DM cases are Type 2
Type 2 DM
 Inception of disease begins with development of
key metabolic abnormality, insulin resistance.

 Integral to understanding of type 2 DM is the role

of insulin/glucose in the metabolic system.
Insulin

 A polypeptide hormone
secreted by the islet of
Langerhans in β-cells of the
pancreas.

 First isolated in 1921 by

Canadian researchers
Banting & Best

 Essential in homeostatic
regulation of blood glucose
Insulin’s function
 Standard metaphor (Lock & Key)
Insulin (the key) must be bound to target cell (the lock) in
order for glucose to enter the target cell from the
bloodstream.
 Homeostatic function
Signals muscle/adipose tissues and liver to absorb glucose
and utilize it. When energy requirements are met, insulin
in the bloodstream triggers the liver to absorb glucose and
convert it into energy saving form glycogen.
Insulin Resistance
 Metabolic abnormality that triggers the onset of
type 2 DM
Normal amount of insulin becomes inadequate for proper
absorption of blood glucose
The body’s energy absorption system becomes inept
 Hypothesized triggers of IR
1 in 10 people have genetic code for IR.
Obesity, Aging, Genetics, Diet high in sucrose/HFCS
Ensuing Hyperglycemia
 Complications
 Symptoms
Vascular problems
(neuropathy, nephropathy, Frequent urination
retinopathy) (polyuria)
Frequent thirst
Cardiovascular disease (polydipsia)
Excessive hunger
Wound infection
(polyphagia)
Type 2 DM Diagnosis
Fasting blood glucose level - diabetes is diagnosed if
higher than 126 mg/dL on two occasions.
Random (non-fasting) blood glucose level - diabetes
is suspected if higher than 200 mg/dL and
accompanied by the classic symptoms of
increased thirst, urination, and fatigue.
Oral glucose tolerance test - diabetes is diagnosed if
glucose level is higher than 200 mg/dL after 2
hours.
Treatment of type 2 DM
 First goal is to eliminate symptoms and stabilize blood
glucose levels.

 If diet/exercise fail, then oral medications are used

 Treatments include
agents which increase the amount of insulin secreted
by the pancreas
agents which increase the sensitivity of target organs
to insulin
agents which decrease the rate at which glucose is
absorbed from the gastrointestinal tract.
Oral Medications Overview

 Sulfonylureas
 Meglitinides
 Biguanides
 Thiazolidinediones
 α-Glucosidase inhibitors
 Dipeptidyl peptidase-
4 inhibitors
Sulfonylureas
 Stimulates insulin
secretion by β cells.
 1st generation
Acetohexamide
 Binds and closes K+ Chlorpropamide
channels on β cells causing
influx of Ca2+ which Tolbutamide
triggers the release of Tolazamide
insulin.
 2nd generation
 Not glucose dependent. Glipizide
Cause insulin release Gliclazide
regardless of glucose level
Glyburide
Glimepiride
Meglitinides
 Also stimulates insulin
secretion by β cells
 Repaglinide
 Similar mechanism of
action to Sulfonylureas.
Attaches to K+ channel at a
different binding site

 Insulin efflux is glucose

dependent. High glucose  Nateglinide
levels are needed for
optimal action.
Biguanides
 Improves insulin’s ability to
move glucose into cells
(particulary in muscle
 Metformin
tissue)

 Exact mechanism of action

is not fully elucidated

 First-line medication used

for treatment of type 2 DM
Thiazolidinediones
 Improves insulin sensitivity (adipose tissue)
 Bind to steroid hormone nuclear receptor family-
peroxisome proliferator activated receptors
[PPARs]- specifically PPARγ isoform.
 Activated PPARγ causes the transcription of
specific genes that are intimately involved in
cellular metabolism.
 Activated genes regulate glucose/fat metabolism
and result in increased insulin sensitivity.
 rosiglitazone (Avandia) pioglitazone (Actos)
α-Glucosidase inhibitors
 Prevents digestion of  Acarbose
carbohydrates

 Thus, they reduce their

impact on blood glucose

 Competitively inhibits  Miglitol

enzymes needed for
carbohydrate digestion
Dipeptidyl peptidase 4 inhibitors
 Causes increased Incretin  Vildagliptin
levels

 Sitagliptin
Drug cocktails
 Combination therapy is sometimes used. Two drugs
combined into one tablet.
 Examples include:

Sulfonylurea + Metformin = Glucovance

+
Metformin + Thiazolidinedione = Metaglip
Future of type 2 DM
 Complications can be prevented through
proper diet and exercise

 Goal of future drug research is normalizing

blood glucose and decreasing insulin resistance

 Proper education is necessary. Majority of

complications are caused by negligence.
Any questions?