Frequently asked Questions
Pathological Anatomy and Physiology Exam – 3rd year
Q: Disorders of cell membrane signaling (receptors and membrane channels) and its
consequences.
A: Question is similar to “Pathophysiology of signal transmission” and part of
“Pathophysiology of receptors in the endocrine system”
Start with Physiology: Signal is transmitted in various systems (neural, immune, and
endocrine)

Where are receptors located? (e.g., neuro: presynaptically, postsynaptically; in
endocrine: on membranes, in cytoplasm, in the nucleus, etc.)

What is the mechanism of signal transport? (e.g., channels)
Pathophysiology:

The receptors can be influenced by various substances or processes (see slide below
– it is for endocrine system – all these situation change membrane signaling): (age,
antibodies (inflammation), etc.)

Consequences: sensitivity changes (especially insulin), change of function (may be
increased or decreased: i.e. by antibodies (agonistic effect of Ab in Graves
Basedow, destruction of receptors in myasthenia gravis, block of receptors in
myasthenic syndrome)
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Level of failure
Receptors
The presence of other
substances acting on
receptors
Mechanism
Genetics (increased or decreased
amount)
Example
Decreased amount of receptors for ADH
in kidneys (inherited Diabetes Insipidus)
Sy of testicular feminization
Genetics – decreased sensitivity of
Laron dwarfism (receptors for
receptors
somatomedins)
Damage (most often by Ab )
Myasthenia gravis
Age 
Sensitivity of rec.
In tumors  (ca mammae)
Obesity -  amount (and also sensitivity)
Up and down regulation
of insulin receptors
Stimulating Ab
Binding to TSH rec.- Basedow’s disease
Asthma bronchiale (Ab block β
Inhibitors Ab
adrenergic rec)
Myasthenia gravis (block
Agonists
Amphetamine (Agonist of dopamine)
Block trypsin receptors -  secretion of
Antagonists
CCK – hypertrophy of pancreas
Grow hormone – galactorrhea in
acromegaly
Hormone spillover
Insulin – hyperandrogenemia
Cortisol – mineralocorticoid effect
Q: Disorders of regulatory mechanisms in the endocrine system
A: Start with physiology: what is necessary for normal hormonal regulation, types of
feedback, example of hormones regulation by simple or complex feedbacks?
The failure of regulation might be due to adenoma (overproduction without regulation
possibility), failure of receptors (normal secretion, no action), failure of channels, G proteins,
protein synthesis, i.e. in decreased amount of substrates due to malabsorption, etc.
Q: Disorders of the hormonal and nervous control in GIT
A: Start with physiology: describe the enteric nervous system, local hormones (from gastrin
to motilin, cholecystokinin, secretin, somatostatin or VIP), influences of sympathetic and
parasympathetic nervous systems, reflexes.
Do not forget the effect of increased thyroid hormones (which increase motility) and
aldosterone (increases reabsorption of water in the large intestine).
Briefly overview, name the disorders and choose one to describe.
The most often consequences of dysregulation in GIT are constipation and diarrhea
Acute diarrhea leads to dehydration, loss of ions, metabolic acidosis; chronic – to
malabsorption sy.
Q: Endocrine causes of mineral metabolism disturbances
A: You can speak about aldosterone that regulates metabolism of sodium, however, be
aware, that it does not change its concentration (one molecule of sodium binds osmotically to
one molecule of water). But aldosterone leads to excretion of potassium in the kidneys.
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ADH (from the posterior pituitary) increases “free” water retention, thus increased ADH (i.e.
in SIADH) decreases concentration (dilutes) all ions but the total amount in the body remains
the same. Decreased secretion of ADH (diabetes insipidus) leads to increased
concentrations of ions.
Depending on the cause of secretion changes of these hormones, different consequences
develop. Describe cause>consequence
Remember: glucocorticoids in overproduction have mineralocorticoid effect.
You can speak also about calcium metabolism and its regulation (PTH, calcitonin, calcitriol).
Q: Endothelial dysfunction
A: Endothelial cells synthesize and release various factors that regulate angiogenesis,
inflammatory responses, hemostasis, as well as vascular tone and permeability.
Endothelial dysfunction has been associated with a number of pathophysiological processes.
Oxidative stress appears to be a common denominator underlying endothelial dysfunction in
cardiovascular diseases. However, additional factors such as age, sex, salt intake,
cholesterolemia, glycemia, smoking, hypertension and hyperhomocysteinemia are the
mechanisms underlying the endothelial dysfunction.
Consequences: hypertension (vasoconstriction due to increased endothelin or decreased NO
production), atherosclerosis (due to increased adhesive molecules and pro-inflammatory
changes in the endoth. cells), formation of thrombi (due to decreased smoothness of the
vessels).
Consequences for the organism: hypertension, ictus, lung embolism, ICHS, heart failure...
Q: Changes in compliance in individual organs
A: Changes of compliance can be seen in the following organs: lungs and chest, heart,
blood vessels, urinary bladder, etc.
The common causes of the changes (decreased compliance) are fibrotisation (e.g., scaring
after MI), inflammation, in vessels it is atherosclerosis and applicable for all organs is
physiological aging.
The consequences are changed functions.
Q: Inborn of defects of glycogen metabolism
A: This is a question from pathology. Be aware: diabetes mellitus is a disease of glucose
metabolism, not glycogen, so as galactose.
Q: Pathophysiology of mineral metabolism (Ca, P)
As to phosphate changes – increase: most often in kidney failure, consequence – decreased
calcium => as feedback increase in PTH secretion and therefore osteoporosis, calcifications,
etc.
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– decrease: caused by high PTH (increases excretion), low calcitriol (no resorbtion of
phosphates in the gut) and phosphate diabetes (loss of phosphate in urine due to failure in
transport mechanism). Consequences: osteomalacia, decreased body metabolism, fatigue
(decreased ATP synthesis)
Regulation together with calcium: calcitriol increases Ca and P; PTH increases Ca,
decreases P.
Q: Pathophysiology of receptors in the endocrine system
A: Start with physiology: where receptors in endocrine system are located (on membranes, in
cytoplasm, in the nucleus...)
What substances or processes might affect them (age, antibodies (inflammation)...), up- and
down-regulation, consequences: sensitivity changes (especially insulin), autoimmune
affection by Ab with agonistic effect (Graves Basedow), etc.
Q: Role of glucocorticoids in the pathologic states
A: Start with physiology: where it is produced, how its production is regulated and when the
production increases and what are the effects.
Talk about stress, Addison´s, Cushing´s (note: Cushing´s sy x Cushing´s disease). Do not
forget the effects on bones (osteoporosis), inflammation, blood pressure and so on.
Q: Smooth muscle dysfunction
A: Physiology: what are the characteristics of smooth muscles; their regulation (autonomic
nervous system, influence of ions, necessity of extracellular calcium for the contraction, own
nervous system in GIT, bladder). Important characteristics are compliance and elasticity.
Pathophysiology: changes of GIT motility (esophageal achalasia, decreased frequency of
stomach emptying in diabetic patients (failure of autonomic nervous system), obstipation –
e.g., ileus with colicky pain; increased motility – diarrhea; Hirschsprung’s disease.
Vessels – hypertension; ureters – obstruction by calculi – colicky pain; urinary bladder –
disorders of emptying with decreased compliance or elastance.
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