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Advanced Pathophysiology Exam 1 | Study Guide & Exam Prep

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Study for Advanced Pathophysiology Exam 1 with focused exam prep resources, key concepts, and review material designed for success.

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1 Advanced Pathophysiology Exam 1


7 possible mechanisms of fatty accumulation -increased movement of free fatty acids into the liver
-Failure of metabolic process that converts fatty acids to phospholipids
resulting in the preferential conversion of the fatty acids to triglycerides
-increased synthesis of triglycerides from fatty acids
-decreased synthesis of apoproteins (lipid acceptors)
-failure of lipids to bind with apoproteins and form lipoproteins
-failure of mechanisms that transport lipoproteins out of the cell
-direct damage to the ER by free radicals released by alcohol's toxic
effects


abnormal substances that cause cell accumulation -endogenous: product of abnormal metabolism synthesis
-exogenous: infectious agent or material


The accumulation of lactic acid that occurs with B
impaired energy production results from which of
the following?
a. increased intracellular glucose
b. increased anaerobic metabolism
c. decreased metabolic rate
d. increased oxidative phosphorylation


acute tubular necrosis damage to the renal tubules due to presence of toxins in the urine or to
ischemia
most common cause of hospital acquired ARF




2/4/2026

,2 Advanced Pathophysiology Exam 1


apoptosis -event that results in cell death
-quiet, organized, programmed process resulting in elimination of
individual cells


Apoptosis death-receptor pathway -Fas and TNF receptor are integral membrane proteins with their receptor
domains exposed at the surface of the cell
-binding of the complementary death activator (FasL and TNF) transmits a
signal to the cytoplasm
-actiavation of caspase 8
-initiates cascade of caspase activation
-phagocytosis of cell


apoptosis-inducing -neurons have another way to self-destruct that does not use caspases
-AIF is a protein that is normally located in the intermembrane space of
mitochondria
-when cell receives death signal, AIF:
-released from mitochondria
-migrates to nucleus
-binds to DNA
-triggers destruction of the DNA and cell death




2/4/2026

,3 Advanced Pathophysiology Exam 1


Apoptosis - mitochondrial pathway -healthy cell - protein Bcl-2 on surface - inhibits apoptosis
-internal damage to cell
-protein Bax migrates to the surface of the mitochondria where it inhibits
protective effect of Bcl-2
-inserts self into outer mitochondrial membrane punching holes in it
-cytochrome c leaks out
-cytochrome c binds to the protein Apaf-1
-complexes aggregate to form apoptosomes
-bind to and activate caspase-9
-cleaves and activates other caspases (executioner ones)
-digestion of structural proteins in the cytoplasm
-degradation of chromosomal DNA
-phagocytosis of the cell


Atrophy Decrease or shrinkage in cellular size.Most common in skeletal muscle,
heart, secondary sex organs, and brain.


calculate the anion gap AG = (Na + K) - (Cl + HCO3)


calculation for corrected serum sodium G= (pt. glucose - 100)/100


(1.6 mEq/L x G) + (serum sodium)


calculation for ideal TBW (current Na X TBW)/140




2/4/2026

, 4 Advanced Pathophysiology Exam 1


Calculation for serum osmolality OSM = 2 X [sodium concentration] + [glucose concentration/18] +
[BUN/2.8]


calculation for water deficit ((current Na X TBW)/140) - TBW


calculation for water excess the difference between current TBW and ideal TBW
water excess =
weight (kg) x (0.5 F) x (1 - (Na/125))
(0.6 M)
(0.7 infants)


calculation of water def the difference between ideal TBW and current TBW =
weight in kg x (0.4 F)
(0.5 M)
(0.6 infants)


caseous necrosis commonly results from tuberculous pulmonary infection
combination of coagulative and liquefactive
the dead cells disintegrate but the debris is not digest completely by
hydrolases
tissues appear soft and granular and resemble clumped cheese




2/4/2026

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Subido en
5 de febrero de 2026
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2025/2026
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