Endocrine Flashcards
Which of the following is correct regarding thyroid hormone?
A Decreases metabolic rate
B Increases Na/K-ATPase function
C Acts on a cell surface receptor
D Has no effect on beta adrenergic receptor numbers
B
Explanation
Thyroid hormone acts on the nucleus and causes an increase in metabolic rate. Thyroid hormone increases both the affinity and the number of beta adrenergic receptors
Which of the following is caused by thyroid hormones?
A Increased number but not affinity of beta adrenergic receptors
B Decreased activity of Na/K ATP-ase
C Thyroid hormones cause increased expression of the of the B-myosin heavy chain
D Increased number of LDL-receptors
D
Explanation
Thyroid hormones cause an increased expression of the A-MHC and a decrease in B-MHC. The converse occurs in hypothyroidism. They increase both the number and affinity of the beta adrenergic receptors. They increase activity of the NA/K-ATPase
Extra:
Thyroid hormones increase the activity of the membrane-bound Na, K ATPase in many tissues. Thyroid hormones Increases both number and affinity of beta adrenergic receptors. Thyroid hormones lower circulating cholesterol levels. The decrease in plasma cholesterol concentration is due to increased formation of low-density lipoprotein (LDL) receptors in the liver, resulting in increased hepatic removal of cholesterol from the circulation. A-MHC predominates in the atria in adults, and its level is increased by treatment with thyroid hormone. This increases the speed of cardiac contraction. Conversely, expression of the A -MHC gene is depressed and that of the B-MHC gene is enhanced in hypothyroidism. Circulatory T3 enters the myocytes, combines with its receptors, and enters the nucleus, where it promotes the expression of some genes and inhibits the expression of others. Those that are enhanced include the genes for A-myosin heavy chain, sarcoplasmic reticulum Ca2+ ATPase, Beta -adrenergic receptors, G proteins, Na- K ATPase, and certain K+ channels. Those that are inhibited include the genes for : B-myosin heavy chain, phospholamban, two types of adenylyl cyclase, T3 nuclear receptors, and NCX, the Na+–Ca2+ exchanger. The net result is increased heart rate and force of contraction.
Which of the following does not utilise the same receptor effector pathway?
A Parathyroid hormone (PTH)
B Glucagon
C Adrenalcorticotrophic hormone (ACTH)
D Insulin
D
Explanation
Glucagon, parathyroid hormone (PTH) and adrenalcorticotrophic hormone (ACTH) all function as extracellular ligands which bind to a receptor and activate the secondary messenger cyclic adenosine monophosphate (cAMP).
Insulin functions via the ligand regulated transmembrane enzyme signaling pathway (tyrosine kinase)
Which of the following is not a gastrointestinal hormone?
A Cholecystokinin (CCK)
B Vasoactive intestinal peptide (VIP)
C Secretin
D Enteropeptidase (EP)
D
Explanation
Enteropeptidase is a brush border enzyme that converts trypsinogen into the active enzyme trypsin. The rest are biological active polypeptides that are secreted by nerve and gland cells in the mucosa and act in a paraendocrine fashion. These gastrointestinal hormones play an important role in gastrointestinal secretion and motility
Note: VIP is first mentioned as part of the secretin family of hormones. These include secretin, glucagon, glicentin and GIP-gastric inhibitory polypeptide. Later on, VIP is further discussed. Because it is found in the nerves in the GIT, it itself is not a hormone but rather a neurotransmitter or neurocrine
Note: the current TB and online sources report EP as an enzyme rather than a hormone. I have found a few source which state that EP is a hormone.
Latest Update: please note: in the current textbook-26 edition: it states: “VIP is found in nerves in the GIT tract and thus is not itself a hormone despite its similarities to secretin. VIP is however found in the blood”
Final: I am not sure of the answer. Given the fact that enteropeptidase-ends in ASE- and enzyme, it may be the correct answer i.e. not a hormone. The national cancer institute reports VIP as a hormone.
Regarding parathyroid hormone (PTH), which of the following statements is correct?
A It is released when there is a rise in blood calcium levels
B Blocks vitamin D synthesis
C It causes a low phosphate (PO4)
D Raises serum Mg
C
Explanation
PTH acts directly on bone to increase bone resorption and mobilize Ca. It also depresses plasma PO4. PTH increases phosphate excretion in the urine, due to a decrease in reabsorption of PO4 in the proximal convoluted tubules
Hypothyroidism results in all of the following except?
A Weight gain
B Early genital development
C Cretinism
D Coarse hair
B
Explanation
Features of Hypothyroidism include
- A decrease in basal metabolic rate of up to 40%
- Hair is coarse and sparse
- The skin is dry and yeollowish
- Cold is poorly tolerated
- The voice is husky and slow
- Mentation is slow and retarted
- weight gain
- Water retension
Cretinism is a condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones (congential hypothyroidism) usually due to maternal hypothyrodism
With regard to cortisol, which of the following statements is false?
A It has a permissive action on vascular reactivity
B It has greater mineralocorticoid activity than glucocorticoid activity
C It is predominantly metabolised in the liver
D 11-deoxycortisol is converted by 11B hydroxylase in the mitochondria to form cortisol.
B
Explanation
Cortisol has glucocorticoid and some mineralocorticoid activity. Dexamethasone has only glucocorticoid activity and aldosterone, which is also a glucocorticoid, has high mineralocorticoid activity.
Note:
Cortisone 17-hydroxy-11-dehydrocorticosterone) is a 21-carbon steroid hormone. Cortisone is one of several end-products of steroidogenesis. This process starts with the synthesis of cholesterol, which then proceeds through a series of modifications in the adrenal gland to become any one of many steroid hormones. One end-product of this pathway is cortisol. 11-deoxycortisol move back into the mitochondria where it is 11-hydroxylated to form cortisol. This reaction occurs in the zona fasciculata and zona reticularis and is catalysed by 11B hydroxylase.
Extra
The principal steroid with mineralocorticoid activity is aldosterone. Cortisol, the major glucocorticoid in non-rodent species, is said to have “weak mineralocorticoid activity”, which is of some importance because cortisol is secreted very much more abundantly than aldosterone. Another way to state this is that a small fraction of the mineralocorticoid response in the body is due to cortisol rather than aldosterone.
The mineralocorticoid receptor binds both aldosterone and cortisol with equal affinity. Moreover, the same DNA sequence serves as a hormone response element for the activated (steroid-bound) forms of both mineralocorticoid and glucocorticoid receptors. An obvious question is:
How can aldosterone stimulate specific biological effects in this kind of system, particularly when blood concentrations of cortisol are something like 2000-fold higher than aldosterone?
A large part of the answer is that, in aldosterone-responsive cells, cortisol is effectively destroyed, allowing aldosterone to bind its receptor without competition. Target cells for aldosterone express the enzyme 11-beta-hydroxysteroid dehydrogenase, which has no effect on aldosterone, but converts cortisol to cortisone, which has only a very weak affinity for the mineralocorticoid receptor. In essence, this enzyme “protects” the cell from cortisol and allows aldosterone to act appropriately. Some tissues (e.g. hippocampus) express abundant mineralocorticoid receptors but not 11-beta HSD - they therefore do not show responses to aldosterone because aldosterone is not present in quantities sufficient to compete with cortisol.
Source: vivo.colostate.edu
Regarding thyroid hormones, which of the following statements is false?
A They increase the activity of Na/K-ATPase
B They alter the proportion of alpha myosin heavy chains
C They increase plasma cholesterol
D They have a calorigenic action
C
Explanation
Thyroid hormones alter the alpha portions of heavy chain. They increase both the number and affinity of the beta adrenergic receptors. They increase activity of the Na/K-ATPase. Thyroid hormones lower circulating cholesterol levels. Thyroid hormones have a calorigenic action-producing body heat
Regarding insulin, which of the following statements is correct?
A Its secretion is inhibited by somatostatin
B Its secretion is stimulated by phenytoin
C It increases protein catabolism in muscle
D It causes decreased K+ uptake into adipose tissue
A
Explanation
Insulin is an anabolic hormone, the net effect of which is storage of carbohydrate, fat and protein. Many substances inhibit insulin including phenytoin. It increase K uptake and is acutely effective in the treatment of hyperkalaemia.
The following cause insulin stimulation:glucose, mannose, amino acids, ACH, glucagon, B adrenergic stimulators, intestinal hormones, B ketoacids, cyclic AMP and sulfonylurease.
Insulin inhibitors include: alpha adrenergic stimulators, somatostatin, 2-deoxyglucose, mannoheptulose, galanin, hypokalaemia, phenytoin, alloxan, microtubule inhibitors, beta blockers, thiazide diuretic, insulin, diazoxide.
Which of the following statements is correct regarding glucagon?
A It increases glycogen formation
B It has a half life 30 minutes
C It is secreted by the pancreatic beta cells
D It stimulates insulin secretion
D
Explanation
Glucagon is secreted by the alpha cells of the pancreas. It stimulates gluconeogenesis to produce glucose. Half life is 5-10min.
The following cause insulin stimulation: glucose, mannose, amino acids, ACH, glucagon, B adrenergic stimulators, intestinal hormones, B ketoacids, cyclic AMP and sulfonylurease.
With regard to thyroid physiology, which of the following statements is correct?
A T4 acts more rapidly on the thyroid receptor than T3
B T4 is synthesised from tyrosine held in thyroglobulin
C T3 and T4 are metabolised in the spleen and bone marrow
D T3 is bound to a complex polysaccharide in the plasma
B
Explanation
Note: the explanation below forms a recall question as well
Normal plasma T4=8ug/dl and plasma T3=0.15ug/dl. Both are relatively lipophilic. Albumin has a greater capacity to bind T4 than TBG, but TBG has a greater affinity. Most of the circulating T4 is bound to TBG. 99.98% of T4 in plasma is protein bound. Free T4=2ng/dl. T1/2=6-7d. Vd=10L.
T3 is less bound (99.8%). 0.3ng/dl is free. It has a shorter half-life then T4 (about 2.5d) and its actions on the tissues is more rapid. Of the T3 that is protein bound, 46% to TBG and the rest to albumin
T3 and T4 are metabolized in the liver and kidneys. They act on nuclei receptors. T3 is more active than T4. T4 and T3 are bound to proteins-albumin, TBG and transthyretin
Extra:
Thyroglobuin is a glycoprotein made up of two subunits and has a molecular weight of 660 kDa. It contains 10% carbohydrate by weight. It also contains 123 tyrosine residues, but only 4-8 of these are incorporated into thyroid hormones.
T3 and T4 (although less avidly than T3) bind to the TR in the nuclei. The hormone receptor complex then binds to DNA via zinc fingers and increases (or in some cases, decreases) the expression of a variety of different genes that code for proteins that regulate cell functions. In most of its actions T3 acts more rapidly and is three to five times more potent than T4. This is because T3 is less tightly bound to plasma proteins than is T4, but binds more avidly to thyroid hormone receptors. As previous noted , RT3 is inert.
99.8% of T3 is protein bound. 46% to TBG and the remainder to albumin. Very little binding to transthyretin
20% of transthyretin is bound to T4
T4 and T3 are deiodinated in the liver, kidneys and many other tissues. These deiodination reactions serve to catabolize the hormones and to provide a local supply of T3. Some of the T4 and T3 is further converted to deiodotyrosinases and some are conjugated in the liver to form sulfates and glucuronides. These products enter the bile and are passed into the intestine. Enteroheaptic circulation reabsorbs some of the conjugates while other are excreted in stool
A deficiency of parathyroid hormone (PTH) is likely to lead to which of the following?
A The formation of kidney stones
B Neuromuscular hyperexcitability
C Hypophosphataemia
D Cystic bone disease
B
Explanation
A lack of PTH will cause a rise in phosphate and a decrease in plasma Ca. PTH causes bone resorption and thus cystic disease and may lead to kidney stones. Hypocalcaemia leads to neuromuscular hyperactivity giving rise to Chvosteks and Trosseaus signs.
With regard to adrenal physiology which of the following statements is correct?
A Cortisol has no mineralocorticoid activity
B The largest steroid molecules are the oestrogens
C Glucacorticoids exert their action by cyclic guanosine monophosphate (cGMP) activation
D Dopamine is secreted by the adrenal medulla
D
Explanation
Glucocorticoids are intranuclear hormones and attach onto nuclear receptors. Cortisol has a predominantly glucocorticoid effect and some mineralcorticoid activity. Oestrogen molecules are only 18C (carbon), testosterone has 19C, progesterone has 21C and cholesterol has 27 C
Insulin secretion is stimulated by all of the following except?
A Noradrenaline
B Leucine
C Glucagon
D Acetylcholine
A
Explanation
Insulin is an anabolic hormone, the net effect of which is storage of carbohydrate, fat and protein. Many substances inhibit insulin including phenytoin. It increase K uptake and is acutely effective in the treatment of hyperkalaemia.
The following cause insulin stimulation: glucose, mannose, amino acids, ACH, glucagon, B adrenergic stimulators, intestinal hormones, B ketoacids, cyclic AMP and sulfonylurease.
Insulin inhibitors include: alpha adrenergic stimulators (NA and adrenaline), somatostatin, 2-deoxyglucose, mannoheptulose, galanin, hypokalaemia, phenytoin, alloxan, microtubule inhibitors, beta blockers, thiazide diuretic, insulin, diazoxide.
NOTE: ANY OF THE ABOVE OPTIONS CAN BE USED TO CREATE THIS QUESTION
Which of the following statements is true regarding insulin?
A Is synthesised as a prohormone
B Binds at cytoplasmic receptor sites
C Is a triple helical polypeptide
D Causes K+ to leak out of cells
A
Explanation
Insulin is a polypeptide containing two chains of amino acids linked by disulphide bridges. It is synthesized in the rough endoplasmic reticulum of the beta cells of the pancreas. Half-life of insulin is 5 -10 min. It is an anabolic hormone, which binds to its transmembrane receptors. Note that insulin receptors are found on many different cells in the body, including cells in which insulin does not increase glucose uptake. Insulin cause the movement of potassium into cells. Like other polypeptide hormones and related proteins that enter the endoplasmic reticulum, insulin is synthesised as part of a larger perprohormone. I.e. preproinsulin-proinsulin-insulin
