Porth online = http://www.scribd.

com/collections/2781108/Essentials-of-Pathophysiology-Porthl

18. http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Hore
%25C4%258Dka_(pediatrie)&rurl=translate.google.cz&twu=1&usg=ALkJrhgIucTAbUYGGC-P7IKDWwK2LFPbOg
http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Reaktanty_akutn%25C3%25AD_f
%25C3%25A1ze&rurl=translate.google.cz&twu=1&usg=ALkJrhgucBIZkDrwycIiFjs4MuqwbFHFHQ
http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Z%25C3%25A1n
%25C4%259Bt&rurl=translate.google.cz&twu=1&usg=ALkJrhi__Dy0XJ6RiMRMVJtrTxDK60R5xw

19.
http://www.wikiskripta.eu/index.php/MODS
http://www.wikiskripta.eu/index.php/Sepsis

20. http://faculty.weber.edu/molpin/healthclasses/1110/bookchapters/stressphysiologychapter.htm
http://www.willamette.edu/cla/biology/resources/biol244/pdf/Stress%20L1.pdf

21. http://www.wikiskripta.eu/index.php/Alergie
http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Anafylaktick%25C3%25BD_
%25C5%25A1ok&rurl=translate.google.cz&twu=1&usg=ALkJrhh_v3VkEXPY_UNFw2wJWF5-fmSv4w

25. http://emedicine.medscape.com/article/906999-overview#a0104
http://www.merckmanuals.com/professional/sec19/ch276/ch276b.html
http://www.wikiskripta.eu/index.php/Poruchy_vodn%C3%ADho_hospod%C3%A1%C5%99stv%C3%AD

26. http://en.wikipedia.org/wiki/Water_intoxication
http://www.wikiskripta.eu/index.php/Natrium

27. http://www.wikiskripta.eu/index.php/Hypoxie
http://www.med.univ-
montp1.fr/enseignement/cycle_2/MIF/Ressources_locales/Urgences/TISSUE_HYPOXIA_.pdf
http://www.hyperbaric-oxygen-info.com/tissue-hypoxia.html
http://www.wikiskripta.eu/index.php/Hypoxie_(podrobn%C4%9B)

28. https://el.lf1.cuni.cz/p91662903?account-id=7&principal-id=892077session=breez7ucy3t3ras58q39c
http://en.wikipedia.org/wiki/Reperfusion_injury#Therapeutic_hypothermia

29. 30. 31.  http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-

8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Laboratorn%25C3%25AD_vy %25C5%25A1et
%25C5%2599en%25C3%25AD_acidobazick%25C3%25A9_rovnov
%25C3%25A1hy&prev=_t&rurl=translate.google.cz&twu=1&usg=ALkJrhjhzhypazFAWmSDg2BFvyOSdVYC8Q
http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-
8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Vztahy_mezi_acidobazickou_rovnov
%25C3%25A1hou_a_ionogramem&prev=_t&rurl=translate.google.cz&twu=1&usg=ALkJrhimjlBcVoF6jqQ_ESMr
DmHCXSpWfg
http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-
8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Kombinovan%25C3%25A9_poruchy_acidobazick
%25C3%25A9_rovnov
%25C3%25A1hy&prev=_t&rurl=translate.google.cz&twu=1&usg=ALkJrhgMBIp6Z1egHgZW8lLkP6QHK7XOcA
http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-
8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Acidobazick%25C3%25A1_rovnov
%25C3%25A1ha&prev=_t&rurl=translate.google.cz&twu=1&usg=ALkJrhhQH4ReWPfncvoIvqJsuAl5OxtY0A
http://che1.lf1.cuni.cz/html/ABR%20angl%20200910.pdf
http://www.scribd.com/doc/25128030/PATHO-CH06-Alterations-in-Fluids-Electrolytes-And-Acid-base-Balance-
Porth pg 108
http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-
8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Principy_l
%25C3%25A9%25C4%258Dby_poruch_acidobazick%25C3%25A9_rovnov
%25C3%25A1hy&prev=_t&rurl=translate.google.cz&twu=1&usg=ALkJrhh3oE46OMUD0z0_j0VKTDiKtnd6fg
32 and 33 is quite trivial
http://ebooks.thieme.com.ezproxy.is.cuni.cz/reader/color-atlas-pathophysiology16671/3/pathophysiology
http://www.scribd.com/doc/25128127/PATHO-CH09-Inflammation-Tissue-Repair-And-Fever-Porth

34.
http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-
8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Mechanismy_vzniku_n%25C3%25A1dor
%25C5%25AF&prev=_t&rurl=translate.google.cz&twu=1&usg=ALkJrhhiusyk4Iz-JAUb4vhspQCN6rmUTw
https://el.lf1.cuni.cz/p34721229?account-id=7&principal-id=892077session=breezmd2g46ouef4g9boe

35.
http://translate.google.cz/translate?js=n&prev=_t&hl=cs&ie=UTF-
8&layout=2&eotf=1&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Mechanismy_rozvoje_n
%25C3%25A1dorov%25C3%25BDch_onemocn%25C4%259Bn%25C3%25AD

36. and 37.

http://translate.google.cz/translate?js=n&prev=_t&hl=cs&ie=UTF-8&layout=2&eotf=1&sl=cs&tl=en&u=http
%3A%2F%2Fwww.wikiskripta.eu%2Findex.php%2FObezita
http://translate.google.cz/translate?hl=cs&sl=cs&tl=en&u=http%3A%2F%2Fwww.wikiskripta.eu%2Findex.php
%2FObezita_(pediatrie)
http://translate.google.cz/translate?hl=cs&sl=cs&tl=en&u=http%3A%2F%2Fwww.wikiskripta.eu%2Findex.php
%2FPodv%25C3%25BD%25C5%25BEiva_a_karen%25C4%258Dn%25C3%25AD_stavy
http://www.differencebetween.net/science/health/difference-between-kwashiorkor-and-marasmus/
http://emedicine.medscape.com/article/123702-overview
http://emedicine.medscape.com/article/984496-overview#showall
http://emedicine.medscape.com/article/985140-overview#a0104
http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Onemocn%25C4%259Bn
%25C3%25AD_z_nadbytku_
%25C5%25BEivin&rurl=translate.google.cz&twu=1&usg=ALkJrhh8rQ0OfHngqFMn_huT32g8pcrpOw

38.http://www.wikiskripta.eu/index.php?title=Speci%C3%A1ln%C3%AD%3AHled%C3%A1n
%C3%AD&search=vitamin
http://www.ext.colostate.edu/pubs/foodnut/09312.html
http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Onemocn%25C4%259Bn
%25C3%25AD_z_nedostatku_
%25C5%25BEivin&rurl=translate.google.cz&twu=1&usg=ALkJrhhN0Nd5zplaJ1vUmxnIhwQAhvICXA#Malnutrice
_z_podv.C3.BD.C5.BEivy

39. http://www.wikiskripta.eu/index.php?title=Speci%C3%A1ln%C3%AD%3AHled%C3%A1n
%C3%AD&search=vitamin
http://en.wikipedia.org/wiki/Vitamin_poisoning
http://www.ext.colostate.edu/pubs/foodnut/09315.html

40. http://www.wikiskripta.eu/index.php/Hyperlipoproteinemie

41. http://translate.googleusercontent.com/translate_c?
hl=cs&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Poruchy_metabolismu_purinu&rurl=translate.goo
gle.cz&twu=1&usg=ALkJrhgyJe5-c0xCVIaLokDjHnkKsZTHNQ

65. http://www.wikiskripta.eu/index.php/Krevn%C3%AD_transf%C3%BAze

78. http://en.wikipedia.org/wiki/Shock_(circulatory)#Pathophysiology
http://www.mhhe.com/biosci/ap/saladin/cardio/reading9.mhtml
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1408911/pdf/annsurg00938-0126.pdf
http://www.mhhe.com/biosci/ap/saladin/cardio/reading9.mhtml

79. http://www.merckmanuals.com/professional/sec19/ch287/ch287a.html#sec19-ch287-ch287a-2043

80. http://www.merckmanuals.com/home/sec03/ch028/ch028d.html
http://www.merckmanuals.com/home/sec03/ch028/ch028b.html
http://www.patient.co.uk/health/Mitral-Stenosis.htm
http://www.patient.co.uk/health/Mitral-Regurgitation.htm

81. http://www.patient.co.uk/health/Aortic-Stenosis.htm
http://www.patient.co.uk/health/Aortic-Regurgitation.htm
http://www.merckmanuals.com/home/sec03/ch028/ch028f.html
http://www.merckmanuals.com/home/sec03/ch028/ch028e.html

82. http://www.patient.co.uk/health/Heart-Valves-and-Valve-Disease.htm
http://en.wikipedia.org/wiki/Valvular_heart_disease WAJIB
http://www.merckmanuals.com/professional/sec07/ch076/ch076i.html CARI yang lain kat atas tu

83. http://www.merckmanuals.com/home/sec03/ch026/ch026b.html
http://www.merckmanuals.com/home/sec03/ch026/ch026c.html
http://www.merckmanuals.com/home/sec03/ch026/ch026d.html
http://en.wikipedia.org/wiki/Cardiomyopathy

84. http://www.merckmanuals.com/professional/sec07/ch073/ch073b.html
http://www.merckmanuals.com/professional/sec07/ch073/ch073a.html
http://www.merckmanuals.com/professional/sec07/ch073/ch073c.html
http://www.wikiskripta.eu/index.php/Ischemick%C3%A1_choroba_srde%C4%8Dn%C3%AD
http://www.wikiskripta.eu/index.php/Ischemick%C3%A9_zm%C4%9Bny_na_elektrokardiogramu

85. http://www.wikiskripta.eu/index.php/Infarkt_myokardu

87. http://www.skillstat.com/PDF/mceCO.pdf
http://www.merckmanuals.com/professional/sec07/ch078/ch078a.html#sec07-ch078-ch078a-1517

88. http://translate.googleusercontent.com/translate_c?hl=cs&ie=UTF-
8&sl=cs&tl=en&u=http://www.wikiskripta.eu/index.php/Arytmie&prev=_t&rurl=translate.google.cz&twu=1&us
g=ALkJrhg4--JawKO6wBLVGJodEACNeTz97Q
http://www.cvphysiology.com/Arrhythmias/A008.htm
89. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/cardiac-
arrhythmias/#s0095
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/cardiology/cardiac-
arrhythmias/#s0020

90. http://www.accessmedicine.com/content.aspx?aID=2901818

91. http://www.accessmedicine.com/content.aspx?aID=2901818

94. http://www.cvphysiology.com/Arrhythmias/A011.htm

95-99 (heart failure) http://www.merckmanuals.com/professional/sec07/ch074/ch074a.html

100. http://jasn.asnjournals.org/content/15/8/1983.long
http://www.cardiab.com/content/5/1/4

101. http://www.ncbi.nlm.nih.gov/pubmed/11041120

103. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2050636/pdf/aco071-020d.pdf
http://www.youtube.com/watch?v=7EBr01piIcc&feature=related

104. http://www.wikiskripta.eu/index.php/Tromb%C3%B3za
http://www.wikiskripta.eu/index.php/Hlubok%C3%A1_%C5%BEiln%C3%AD_tromb%C3%B3za
http://www.wikiskripta.eu/index.php/Plicn%C3%AD_embolie

105. http://en.wikipedia.org/wiki/Chronic_venous_insufficiency
http://en.wikipedia.org/wiki/Lymphedema

106. Breathing reflexes

Cough Reflex
The bronchi and
trachea are so
sensitive to light
touch that very slight
amounts of foreign
matter or other
causes of irritation
initiate the cough
reflex. The larynx and
carina (the point
where the trachea
divides into the
bronchi) are
especially sensitive,
and the terminal
bronchioles and even
the alveoli are
sensitive to corrosive
chemical stimuli such
as sulfur dioxide gas
or chlorine gas.
Afferent nerve
impulses pass from
the respiratory
passages mainly
through the vagus
nerves to the
medulla of the brain.
There, an automatic
sequence of events is
triggered by the
neuronal circuits of
the medulla, causing
the following effect.
First, up to 2.5 liters
of air are rapidly
inspired. Second, the
epiglottis closes, and
the vocal cords shut
tightly to entrap the
air within the lungs.
Third, the abdominal
muscles contract
forcefully, pushing
against the
diaphragm while
other expiratory
muscles, such as the
internal intercostals,
also contract
forcefully.
Consequently, the
pressure in the lungs
rises rapidly to as
much as 100 mm Hg
or more. Fourth, the
vocal cords and the
epiglottis suddenly
open widely, so that
air under this high
pressure in the lungs
explodes outward.
Indeed, sometimes
this air is expelled at
velocities ranging
from 75 to 100 miles
per hour.
Importantly, the
strong compression
of the lungs collapses
the bronchi and
trachea by causing
their
noncartilaginous
parts to invaginate
inward, so that the
exploding air actually
passes through
bronchial and
tracheal slits. The
rapidly moving air
usually carries with it
any foreign matter
that is present in the
bronchi or trachea.
Sneeze Reflex
The sneeze reflex is
very much like the
cough reflex, except
that it applies to the
nasal passageways
instead of the lower
respiratory passages.
The initiating
stimulus of the
sneeze reflex is
irritation in the nasal
passageways; the
afferent impulses
pass in the fifth
cranial nerve to the
medulla, where the
reflex is triggered. A
series of reactions
similar to those for
the cough reflex
takes place; however,
the uvula is
depressed, so that
large amounts of air
pass rapidly through
the nose, thus
helping to clear the
nasal passages of
foreign matter.

Cough
http://www.merckmanuals.com/professional/sec05/ch045/ch045c.html?qt=cough&alt=sh

107. Alveolar hypoventilation (contrast with pulmonary ventilation)

Alveolar hypoventilation is defined as insufficient ventilation leading to an increase in PaCO2 (ie, hypercapnia).
http://emedicine.medscape.com/article/304381-overview
Regulation of breathing Costanzo 223
http://www.wikiskripta.eu/index.php/Ventila%C4%8Dn%C3%AD_selh%C3%A1n
%C3%AD_(patofyziologie)#Ventilace

108.
http://www.wikiskripta.eu/index.php/Ventila%C4%8Dn%C3%AD_selh%C3%A1n
%C3%AD_(patofyziologie)#Perfuze short-circuit is shunt
mcphee 217
costanzo 220
http://video.about.com/lungcancer/Atelectasis.htm (atelectasis)
impaired perfusion
1. emboli
2. venous congestion
3. reduced pulmonary bed
4. spasm after hypoxia

109. costanzo 202

Impairment in diffusion
1. low n of alveoli
2. increased distance - emphysema
3. increased thickness
Single-breath diffusing capacity
The subject takes a deep breath of 0.3% carbon monoxide (CO) and holds the breath for 10 s before exhaling
and alveolar sampling. During the breath holding, CO is taken up by the haemoglobin of the passing blood in
proportion to its alveolar tension (PACO).
A simple assumption is that the CO uptake is directly proportional to the mean alveolar PCO (symbolised with
PACO). The diffusing capacity of the lung (DL)  is also called the transfer factor, because DL measures not only
diffusion, but the barrier thickness and ventilation-perfusion mismatch as well. Patients with lung disease often
have abnormal size and thickness of the alveolar barrier or ventilation-perfusion mismatch. In such cases
measurement of the CO transfer need not be a true measure of the total diffusing capacity.
Box 14-2: Diffusing capacities of the lungs for
different gasses in healthy persons
ml STPD min-1
Units ml STPD s-1 kPa-1
mmHg-1
Rest Exercise Rest Exercise
DLCO 3 7.5 25 62.5
DL02 3.6 9 29 73
DLCO2 70 175 565 1412
The single-breath CO diffusing capacity is normally 3 ml STPD s-1  kPa-1 at rest. The values during rest and
exercise - and in two units - are shown in Box 14-2.
The transfer factor  is reduced by diseases affecting the lung parenchyma, such as  emphysema,
pneumonectomy and fibrotic diseases (the alveolar barrier is too small in area or too thick or both).

110. http://emedicine.medscape.com/article/167981-overview#a0104
http://www.thoracic.org/clinical/critical-care/clinical-education/respiratory-failure-mechanical-ventilation.pdf
better
http://medind.nic.in/iad/t03/i5/iadt03i5p360.pdf macam best
http://en.wikipedia.org/wiki/Respiratory_failure#Types
http://www.cuhk.edu.hk/med/ans/Trainee%20Manual/Respiratory%20Problems/Respiratory%20failure.pdf
pun OK
Hypoxic respiratory failure that is caused by ventilation-perfusion mismatch with increased pulmonary failure
or short circuit diffusion of membrane alveolocapillary = alveolocapillary block. This type of mixing leads to
intrapulmonálnímu venous and arterial blood. The result is hypoxia with normokapnií since, as already
mentioned above, the solubility of CO 2 is significantly higher than O 2 . Even when the compensatory increase
in ventilation (especially in children increased respiratory rate), we initially found and hypercapnia. With the
deepening of this disorder, but gradually increasing the value of PCO2 in severe conditions has found a global
respiratory insufficiency.
The second type is hypercapnic-hypoxic respiratory failure. It occurs also in the reduction of alveolar ventilation
in relation to the physiological needs of the organism. The result is hypoxia and hypercapnia at the same time.
• disease of the lung parenchyma and to reduce the V / Q ratio initially hypoxic lead to respiratory failure.
• disease of the airways and respiratory control unit to lead-hypercapnic hypoxic respiratory failure.
Hypercapnia is quite typical for the disease currently affecting the respiratory pump.

111. Restrictive, mcphee 230

Fibrosing x Granulomatous x Eosinophilic x Smoking related

Lung fibrosis
Costanzo483

112. Costanzo 484

Asthma
Ch Bronchitis
Emphysema
Bronchiectasis
Involved bronchi are dilated, inflamed, and easily collapsible, resulting in airflow obstruction and impaired
clearance of secretions.

113. COPD mcphee227

http://www.merckmanuals.com/professional/sec05/ch049/ch049a.html

114. Emphysema See above

115. Bronchial Asthma - a triad of intermittent and reversible airway obstruction, chronic bronchial
inflammation with eosinophils, and bronchial smooth muscle cell hypertrophy and hyperreactivity
http://www.merckmanuals.com/professional/sec05/ch048/ch048a.html

116. Atelectasis AState572

Atelectasis refers to collapse of part of the lung.
http://emedicine.medscape.com/article/1001160-overview#a0101
http://www.youtube.com/watch?v=VQRggeFb_J0&feature=related

Pulm. Edema
mcphee233

Pneumonia
Costanzo508 Robbins 508

117. http://www.wikiskripta.eu/index.php/Plicn%C3%AD_fibr%C3%B3za
Idiopathic, professional, post radioactive, systemic conn tiss diseases http://www.wikiskripta.eu/index.php/Syst
%C3%A9mov%C3%A1_onemocn%C4%9Bn%C3%AD_pojiva

118. AState 593 and 595 for Acute Resp Failure

119.
Pneumothorax AState570

120. Aspiration of object/fluids into lungs

http://en.wikipedia.org/wiki/Pulmonary_aspiration
http://www.tbzmed.ac.ir/hospitals/SHAHID%20MADANI/pages/FARSI/aspirationhtm.htm
http://www.merckmanuals.com/professional/sec05/ch052/ch052f.html
Upper Resp Tract Obstruction
http://www.nlm.nih.gov/medlineplus/ency/article/000067.htm
http://www.nlm.nih.gov/medlineplus/ency/imagepages/1098.htm
http://en.wikipedia.org/wiki/Choking

121. Pulmonary embolism

AState589
http://www.merckmanuals.com/professional/sec05/ch050/ch050a.html?qt=pulmonary%20embolism&alt=sh
http://www.wikiskripta.eu/index.php/Plicn%C3%AD_embolie
Differentiate tachypnea and dyspnea (one is subjective)

122.
Oxygenotherapy
LNotes Prof. Necas
http://en.wikipedia.org/wiki/Hyperbaric_oxygen_therapy
Because the hemoglobin of the red blood cells is almost saturated with oxygen under atmospheric
pressure, this route of transport cannot be exploited any further. Oxygen transport by plasma, however is
significantly increased using HBOT as the stimulus.
Mechanical support of Lung Ventilation
http://en.wikipedia.org/wiki/Mechanical_ventilation
Negative vs Positive machines

123.
Oliguria http://www.wikiskripta.eu/index.php/Oligourie
Polyuria http://www.wikiskripta.eu/index.php/Polyurie
Anuria http://www.wikiskripta.eu/index.php/Anurie
Isostenuria http://en.wikipedia.org/wiki/Isosthenuria
http://www.google.cz/url?sa=t&source=web&cd=1&sqi=2&ved=0CB0QFjAA&url=http%3A%2F
%2Fwww.hartnell.edu%2Ffaculty%2Fawright%2Fpowerpoint%2Fb11urinary.ppt&rct=j&q=disturbance%20of
%20urine%20production
%20ppt&ei=ILbRTePeDoPFswbn6NSjCQ&usg=AFQjCNFPNI7dm5rBFSw0_0dYsTV6UA9d6Q&sig2=GKjkODEu2rXe
z2QIytu5qw&cad=rja
http://www.wikiskripta.eu/index.php/Vy%C5%A1et%C5%99en%C3%AD_mo%C4%8Di
Acute tubular necrosis - Pat Illustrated 477
124. Causes of renal failure - classified McPhee 444
Prerenal
Renal
Postrenal

125. Disturbance of glomerular functions - Astate 620, mcphee 455, Class notes
Glomerulopathies = Primarily nephrotic + Primarily nephritic
Astate 620 > There r 5 of them - Nephrotic, nephritic, glomerulonephritis (rapidly progressive + chronic),
asymptomatic. 1 for association with systemic disease.
Pat Illus 454
http://www.merckmanuals.com/professional/sec17/ch235/ch235a.html
Proteinuria
http://www.wikiskripta.eu/index.php/Proteinurie
Nephrotic syndrome
http://www.wikiskripta.eu/index.php/Nefrotick%C3%BD_syndrom

126. Pat ill 476

AState 643
http://www.merckmanuals.com/professional/sec17/ch236/ch236b.html?qt=acute%20tubular
%20necrosis&alt=sh
http://www.wikiskripta.eu/index.php/Akutn%C3%AD_selh%C3%A1n
%C3%AD_ledvin#Akutn.C3.AD_parenchymat.C3.B3zn.C3.AD_ren.C3.A1ln.C3.AD_selh.C3.A1n.C3.AD_.28akutn.C
3.AD_tubul.C3.A1rn.C3.AD_nekr.C3.B3za.29

127. Acute renal failure

AState641 Mcphee449
http://www.merckmanuals.com/professional/sec17/ch233/ch233b.html?qt=acute%20renal%20failure&alt=sh
http://www.wikiskripta.eu/index.php/Akutn%C3%AD_selh%C3%A1n%C3%AD_ledvin

128.
Chronic renal failure AState645 + Figure26-4
http://www.wikiskripta.eu/index.php/Chronick%C3%A9_selh%C3%A1n%C3%AD_ledvin
http://www.merckmanuals.com/professional/sec17/ch233/ch233c.html
Uremia Astate650
http://www.wikiskripta.eu/index.php/Uremick%C3%BD_syndrom
http://en.wikipedia.org/wiki/Uremia

129. ?
AState650

130.
Acquired or both
http://www.merckmanuals.com/professional/sec17/ch237/ch237e.html Renal glycosuria
http://www.merckmanuals.com/professional/sec17/ch237/ch237f.html?qt=renal%20tubular
%20acidosis&alt=sh  or http://www.anaesthesiamcq.com/AcidBaseBook/ab8_5.phpRTAcidosa
http://www.merckmanuals.com/professional/sec17/ch237/ch237d.html nephrogenic DIns
http://www.merckmanuals.com/professional/sec17/ch237/ch237b.html Fanconi Syn
http://www.merckmanuals.com/professional/sec17/ch237/ch237c.html Liddle Syn

Congenital
http://www.merckmanuals.com/professional/sec19/ch291/ch291c.html cystinuria
http://www.merckmanuals.com/professional/sec19/ch291/ch291e.html hypoP rickets (Vit D resistant)
http://www.merckmanuals.com/professional/sec19/ch291/ch291d.html Hartnup
http://www.merckmanuals.com/professional/sec19/ch291/ch291b.html Bartter Syndrome

131.
Due to uremia
mcphee452, Astate650
Due to everything
http://www.upstate.edu/courseware/casestudy/ms2/renaldisease/supplemental/renal%20failure
%20handout.pdf

132. ????

133. http://www.wikiskripta.eu/index.php/Vy%C5%A1et%C5%99en%C3%AD_funkce_ledvin
Costanzo291
SIADH, DInsi, Water drinking and deprivation

134. Urolithiasis
http://www.wikiskripta.eu/index.php/Uroliti%C3%A1za
mcphee459

135.
Dental Caries
Paradontosis
SN bro handsome haha!
Salivation Disorder

159. http://www.merckmanuals.com/professional/sec12/ch150/ch150b.html
Example of receptor disease
http://en.wikipedia.org/wiki/Nephrogenic_diabetes_insipidus
http://www.wikiskripta.eu/index.php/Inzulinov%C3%A1_rezistence
http://www.wikiskripta.eu/index.php/Nefrogenn%C3%AD_diabetes_insipidus
PseudohypoPTH
VitDreceptor defect
Hereditary vitamin D resistant rickets (HVDRR)
http://medind.nic.in/jac/t02/i1/jact02i1p65.pdf for more
Example of gland disorder
http://en.wikipedia.org/wiki/Hashimoto's_thyroiditis
160.
Function of hypothalamus, it’s integration of CNS and endocrine - 523 McPhee
Example - Sympa + RAAldosteron with ADH
Physiology - pg387 Costanzo
Precoccious puberty - 792AState
http://www.wikiskripta.eu/index.php/Nemoci_hypotalamo-hypofyz%C3%A1rn%C3%ADho_syst%C3%A9mu

161.
Lecture notes
Hypopituitary
Low of one or more pit hormone
LH FSH > TSH > ACTH deficit hierarchy onstart of hypopit (but in autoimmune it's the other way
around
Etiology
Iatrogenic (post surgical right after injury  or post radiation after several years)
Invasive - tumor
Inflammation
Infarction
Sarcoidosis
Immunologic disorder
Idiopathy
Manifestation
GH : short, hypoglycemia in adult
ACTH : Addison - hypoglycemia, postural hypotension, low Na, anemia, hyperkalemia
TSH : center hypotyreosis, anemia, hypercholesterol myxedema
LH,FSH : eunuchoid habitus, infertility, osteoporosis
Hypothalalmo pituitary links : prolactin elevation. Tumor in stalk, increased PRL production and
decrease of other hormones
ISOLATED HYPOPITUITARY
KALLMAN SY
ISOL GH DEFICIENCY - CONGENITAL, EMOTIONAL, IDIOPATHIC
MONOTOPIC TRH DEFINCIENCY

F tests for pituitary

Hypofuction > stimulatory test
Hyperfunction > inhibitory test
Principals :
Negative feedback inhibition or stimulation
Direct stimulation and inhibition
 Dopamine prolactin
ACTH and cortisol
Insulin hypoglycemia test http://www.uptodate.com/contents/insulin-induced-hypoglycemia-test
Very low dose of insulin is administered > hypoglycemia
Stimulates ACTH and GH secretion
Norm: GH >10ng/mL
Negative feedback
Methyrapone test
Levodopa test
Direct
Argini infusion test
TRH test
CRH test
Dopimanergic drugs test (therapeutic values) in prolactin

162.
Gigantism + Acromegaly Altered state pg780
http://www.merckmanuals.com/professional/sec12/ch151/ch151f.html
Acromegaly and gigantism
Different in child and adult

Etiology
Adenoma and carcinoma

Pathogenesis
GH - anti insulin + growth promoting effects

Manifestation
*** in cushing, all is reversible, in acromegaly it's irreversible.

Insulin hypoglycemia test http://www.uptodate.com/contents/insulin-induced-hypoglycemia-test

Very low dose of insulin is administered > hypoglycemia
Stimulates ACTH and GH secretion
Norm: GH >10ng/mL

Lab findings
GH must be measure repeatedly (diurnal rhythm)
IGF - best measure (not diurnal!)
Prolactin also increased
Others cari
DInsipidus AState 171
http://www.wikiskripta.eu/index.php/Diabetes_insipidus
Diabetes Insipidus
Vasopressin deficiency
ADH is a peptide
V1 in blood vessel, V2 in kidney, V3 in APituitary > release of corticothropin
Etiology
A. Central - hypothalamic (VP decrease)
Surgery
Inflammation, tumors, idiopathic
B. Peripheral -nephrogenic (kidney not responsive to VP)
Chronic renal failure (first sign for it is DI)
Congenital abnormalities
Receptor toxicity - lithium
Pulsatile - measurement in one is impossible
Manifestation
Polyuria
Weight loss
headache, thirst
Lab
Plasma hyperosmolarity
Urine hypoosmolarity (below 300)
Abnormal concentration test (36hrs)
Concentration test with ADH administration
Adiuretin/desmopressin (V2 receptor in kidney) administration (treatment of central DI and test)
If no response = nephrogenic
Response - central Diabetes insipidus

163.
Hyperthyroid
LN Dr. Maruna
http://www.merckmanuals.com/professional/sec12/ch152/ch152e.html#sec12-ch152-ch152e-239
http://www.wikiskripta.eu/index.php/Hypertyre%C3%B3za
http://en.wikipedia.org/wiki/Hyperthyroidism#Symptoms_and_signs
Etiology
Hyperthyroidism may result from increased synthesis and secretion of thyroid hormones (thyroxine [T4] and
triiodothyronine [T3]) from the thyroid, caused by thyroid stimulators in the blood or by autonomous thyroid
hyperfunction. It can also result from excessive release of thyroid hormone from the thyroid without increased
synthesis. Such release is commonly caused by the destructive changes of various types of thyroiditis. Various
clinical syndromes also produce hyperthyroidism.

Grave’s disease
http://www.wikiskripta.eu/index.php/Gravesova-Basedowova_nemoc

164. Hypothyroid http://www.wikiskripta.eu/index.php/Hypotyre%C3%B3za

Hypothyroidism is thyroid hormone deficiency. It is diagnosed by clinical features such as a typical facies, hoarse
slow speech, and dry skin and by low levels of thyroid hormones. Management includes treatment of the cause
and administration of thyroxine.
Secondary = Q160?
LN Dr. Maruna
http://en.wikipedia.org/wiki/Myxedema_coma or http://www.wikiskripta.eu/index.php/Myxed%C3%A9mov
%C3%A9_k%C3%B3ma
http://www.merckmanuals.com/professional/sec12/ch152/ch152d.html (Hashimoto’s Disease)
Dif Dx http://www.merckmanuals.com/professional/sec12/ch152/ch152c.html (Euthyroid Sick Syndrome)
Other euthyroid diseases - mcphee 565

165. Inflammation of thyroid

http://www.merckmanuals.com/professional/sec12/ch152/ch152d.html (Hashimoto’s Disease)
Robbins 760

Goiter - mcphee 563

http://www.wikiskripta.eu/index.php/Nemoci_%C5%A1t%C3%ADtn%C3%A9_%C5%BEl%C3%A1zy_s_eutyre
%C3%B3zou

Clinical Features
The dominant clinical features of goiter are those caused by the mass effects of the enlarged gland. In addition
to the obvious cosmetic problem of a large neck mass, goiters may also cause airway obstruction, dysphagia,
and compression of large vessels in the neck and upper thorax. In a minority of patients, a hyperfunctioning
("toxic") nodule may develop within a long-standing goiter, resulting in hyperthyroidism. This condition, known
as Plummer syndrome, is not accompanied by the infiltrative ophthalmopathy and dermopathy of Graves
disease. Less commonly, goiter may be associated with clinical evidence of hypothyroidism. Goiters are also
clinically significant because of their ability to mask or to mimic neoplastic diseases arising in the thyroid.

166.  mcphee 469 (regulation), 476 (hyper), 481 (hypo)

Table 17-9
mcphee very good

167.
physiology mcphee 578
mcphee 594
3 ions affected by aldosteron + Ca also (due to alkalosis)
hypokalemic nephropathy - http://jasn.asnjournals.org/content/19/1/125.full or Hypokalemic nephropathy:
vacuolation of the epithelial cytoplasm of renal convoluted tubules in people seriously depleted of potassium;
vacuoles do not contain fat or glycogen, concentrating ability is impaired, polyuria and polydipsia are common,
and pyelonephritis may develop. SYN: vacuolar nephrosis.

168. mcphee 580

http://www.wikiskripta.eu/index.php/Cushing%C5%AFv_syndrom
http://www.merckmanuals.com/professional/sec12/ch153/ch153e.html?qt=cushing&alt=sh
Clinical manifesation sangat banyak
Cushing sy
Hypercorticalism with hyperproduction of  cortisol
Variant
Cushing disease
Corticoid in plasma is
Low
Pulsative
 Etiology
ACTH dependant
Pituitary (3mm cancer)
Paraneoplastic (small cell carcinoma)
Carcinoid
ACTh independant
Peripheral - adrenal adenoma, hyperplasia, carcinoma
Iatrogenic  (in corticoid treatment = asthma for example)
Manifestation
Endocrine signs - obesity of central
DM
Moon-face
Hypertension
Peptic ulcer
Striae
Osteoporosis ( opposite to vitamin D action)
Moon face central obesity
Lab findings
Plasma levels of cortisol is very dynamic (high during day, low at night (difficulty to interpret) = one
reading is not diagnosis.
Repeated calculation in every few hours
Better to use urine cortisol
Cushing could even have high level of cortisol at night (when it should not)
ACTH can use one time measurement?
Test http://www.merckmanuals.com/media/professional/pdf/Table_153-2.pdf (for results)
Suppressive dexamethasone (low dose vs high dose)
http://en.wikipedia.org/wiki/Dexamethasone_suppression_test or
http://www.merckmanuals.com/professional/sec12/ch153/ch153e.html?
qt=cushing&alt=sh#sec12-ch153-ch153e-462
Methyrapone test (also for Tx of adrenal insufficiency) http://en.wikipedia.org/wiki/Metyrapone
may aid in verifying the cause of Cushing's syndrome. Most patients with pituitary dysfunction
and/or pituitary microadenoma will increase ACTH secretion in response to metyrapone, while
most ectopic ACTH-producing tumors will not. Pituitary macroadenomas do not always respond to
metyrapone.
ACTH test http://en.wikipedia.org/wiki/ACTH_stimulation_test

169 Adrenogenital syndrome = adrenal virilisation = CAH

http://en.wikipedia.org/wiki/Congenital_adrenal_hyperplasia
http://www.wikiskripta.eu/index.php/Adrenogenit%C3%A1ln%C3%AD_syndrom (important)
http://www.merckmanuals.com/professional/sec12/ch153/ch153d.html
mcphee 598 bagus

170. http://www.merckmanuals.com/professional/sec12/ch153/ch153b.html
http://www.wikiskripta.eu/index.php/Addisonova_choroba mcm salah sikit. Sebab addison is primary, so
shouldn’t have central causes.
Everything that got name is primary

171. Pheocromocytoma - Adrenal medulla disorder. mcphee 315

http://www.wikiskripta.eu/index.php/N%C3%A1dory_neuroektodermov%C3%A9#Feochromocytom
http://www.merckmanuals.com/professional/sec12/ch153/ch153h.html
http://en.wikipedia.org/wiki/Clonidine#Clonidine_suppression_test

172. http://www.wikiskripta.eu/index.php/Cukrovka
mcphee 505
DM1
http://www.wikiskripta.eu/index.php/Diabetes_mellitus_1._typu_(biochemie)
http://www.wikiskripta.eu/index.php/Diabetes_mellitus_1._typu_(endokrinologie)
Type 1 DM (10-15%)
Absolute deficiency
Ketoacidosis
Insulin dependant - need insulin therapy
Related to juvenile diabetes = Incidence peaked at 5-7 years old
Quick progression into ketoacidosis > coma
Etiology
Autoimmune (acquired + genetic disposition)
May be started by viral infection of beta cells > destruction
Insulitis - in young diabetics
Normal - infilitration - hydropic changes finally fibrosis
Genetic
Disposition by MHC on 6p chromosome - like hashimoto's disease
Some are protective against DM also!!!
Special type 1
LADA - a late onset
Like type 2 too, but no obesity
Still low insulins and c peptide
Auto Ab present
Tendency to ketoacidosis

Symptoms of insuff activity of insulin

Low glu uptake
Gluconeo in liver and kidney inc
Inc glycogenlysis
Hyperglycemia, hyperplasmaosmolarity
Glycosuria (>10mM???)
Dehydration, Na and K loss
Inc lipolysis
Low lipogenesis
Inc ketoacidosis, acetonuria
Is possible only if insulin production is 0
As insulin can block ketogenesis, thus this (DKAcidosis):
Can be seen in DM type I ONLY!!!!!!
Acute and chronic complications - eye, brain, vessel, kidney

Lab
Glycemia
!!! In stress or infection = cathecolamines increases glycemia (false positive)
Glycated albumin and hemoglobin (long term study)
 A nonenzymatic process
Glc + Protein <> Schiff (reversible)
>ketoamine
>glycated protein
!!!Irreversible in the end
C peptide
Not destroyed while insulin is destroyed
Info of insulin production and release into plasma
To distinguish type 1 from type 2
Urine
Glycosuria
Aceton - ketoacidosis
Proteinuria (nephrotic syndrome etiologic factor - the most usual factor is DM!!!)
Microalbuminuria
U-glucosaminidase - mark of kidney disease
Auto Ab against
B cell
GADecarboxylase - enzyme for GABA production = specific for DM1
Insulin - see whether there is ab against insulin)
Bovine albumin
Marker of micorangiopathy
tPActivator
vWfactor
PAInhibitor activator
DM complications
Acute
Hypoglycemia (overdoses p.o therapy or insulin injection = iatrogenic)- can also be coma PAD,
Insulin
Hyperosmolar hyperglycemic coma DM2
Ketoacidotic coma DM1
Lactoacidotic coma Biguanid therapy (hydrosis) (group of antidiabetic drugs - iatrogenic)
Chronic
Specific
Microangipathy = diabetic leg
Neuropathy - loss of sense, amyotrophy
Eye - cataract, glaucoma, paresis
Renal - sclerosis, albuminuria
Cardiomyopathy - hypertrophy, cardiac dilation
Retinopathy
4 degrees I, II, III, IV (total destruction)
Chronic
Immunoallergic
Diff diagnostics of hypoglycemia
DM - diet mistake, therapy
Insulinoma (50-60% malignant)
Alcohol
Postprandial (alcohol, dumping syndrome ded.= after eating increase absorption of glucose)
http://en.wikipedia.org/wiki/Gastric_dumping_syndrome
Reactive hypoglycemia or late dumping results from rapid emptying of carbohydrates from the gastric
pouch. Early high peaks in blood glucose stimulate excess release of insulin, which leads to symptomatic
hypoglycemia several hours after the meal. A high-protein, low-carbohydrate diet and adequate caloric
intake (in frequent small feedings) are recommended.
Tumor
Liver failure terminal phase
Glycogenoses 1,3,6

Complications - acute (NKHC, KAC, Hypoglycemic Coma)

http://www.wikiskripta.eu/index.php/Akutn%C3%AD_komplikace_diabetu
http://en.wikipedia.org/wiki/Nonketotic_hyperosmolar_coma
http://en.wikipedia.org/wiki/Diabetic_ketoacidosis (Usually in DM1, as in DM2, insulin is present to block
lipolysis)

Complications - chronic
http://www.wikiskripta.eu/index.php/Chronick%C3%A9_komplikace_diabetu

Impaired Glu tolerance

http://www.wikiskripta.eu/index.php/Poru%C5%A1en%C3%A1_gluk%C3%B3zov%C3%A1_tolerance
http://www.wikiskripta.eu/index.php/Poru%C5%A1en%C3%A1_glykemie_nala%C4%8Dno (impaired fasting
glucose - prediabetes)

Oral Glu Tol Test

http://www.wikiskripta.eu/index.php/Orální_glukózový_toleranční_testa
http://www.wikiskripta.eu/index.php/Soubor:Hodnocen%C3%AD_glykemie.png

173.
DM2 http://www.merckmanuals.com/professional/sec12/ch158/ch158b.html?qt=diabetes
%20melitus&alt=sh#sec12-ch158-ch158b-1115
Type 2 DM (80-90%)
Character
Relative lack of insulin
No ketoacidosis
After 30yrs usually (increased after age 30)
Slow
Chronic complications
Etiology and pathogenesis
Genetic and acquired
Genetic - 15-20% only, often familial, polygenic transmission, not all gene is known
Acquired - 80% is obese, overeating, stress, age, inactivity 2a. Type 2b without obesity
Insulin resistance (result of acquired factors) - low receptor low affinity to receptor, post receptor
blockade of part of the signal transduction)
Insulin deficiency (genetic causes) - low maximal insulin secretion to adapt with need
Special
Mody http://en.wikipedia.org/wiki/Maturity_onset_diabetes_of_the_young (like type 2 in effects,
but monogenic!!)
The severity of the different types varies considerably, but most commonly MODY acts like a very
mild version of type 1 diabetes, with continued partial insulin production and normal insulin
sensitivity. MODY is not type 2 diabetes in a young person, as might erroneously be inferred from
the name.
 Not insulin dependant
Opposite of LADA (like type 1) in terms of age of onset

Reaven’s Syn
http://www.merckmanuals.com/professional/sec01/ch006/ch006c.html
Syndrome of insulin resistance
Reaven's syndrome, syndrome x, metabolic syndrome
5 Hs
Obesity (central type)
HLP IV (hyperTAG)
Hypertension
Hyperuricaemia
Atherosclerosis
Coronary disease
DM2nd type
!!!!!>>>>atherosclerosis
Etiology
Postreceptor blockade of insulin influence on musculature (muscles have 80% insulin receptor)
Mechanism?
Defect of Phosphorylation?
IRS-1?
Membrane transport?
Glycogengenesis?
Maybe combined
Pathogenesis
postReceptor blocaked
Low glu uptake >>>> DM2
Stim of b cells
Compensatory hyperinsulinemia
Partial blockade of insulin effects and partial overexpresion of insulin effects
Inc of PAI type one
Prolif of vessel smooth muscle
Na retention
ET1 increased
Sympa activated
Vasocon
Inhibition of NO
>>>> hypertension
HDL and LDL disbalance >>>Dyslipidemia >>> atherosclerosis
Fat tissue is also endocrinacly active
Related to insulinoresistance
?FFA
?TNF
?leptin insufficiency
?cortisol (cushing is like reaven's syndrome)
Physilogical effect of Insulin
http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/pancreas/insulin_phys.html

174. Hypoglycemia http://www.merckmanuals.com/professional/sec12/ch158/ch158f.html?

qt=hypoglycemia&alt=sh
Hyperglycemia (Acute and Chronic complications)

175. 176. See above yo!

179. Male infertlity mcphee 634

Female infertility mcphee 624

238. Test of anterior and post hypophysis

http://www.wikiskripta.eu/index.php/Vy%C5%A1et%C5%99en%C3%AD_funkce_hypof%C3%BDzy

239. Test of thyroid gland AState 785

http://www.wikiskripta.eu/index.php/Vy%C5%A1et%C5%99en%C3%AD_funkce_%C5%A1t%C3%ADtn%C3%A9_
%C5%BEl%C3%A1zy
http://www.wikiskripta.eu/index.php/Vy%C5%A1et%C5%99en%C3%AD_u_chorob_%C5%A1t%C3%ADtn
%C3%A9_%C5%BEl%C3%A1zy