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Flashcards in Physiology 2 Deck (39)
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1
Q

What is the effect of prolonged insulin on insulin receptors?

A

Downregulates

2
Q

What are the two clinical pictures of an insulinoma?

A

Hypoglycemia initially, then hyperglycemia later on d/t downregulation of the receptors

3
Q

What is the serum protein that binds to cortisol?

A

Transcortin

4
Q

What is the effect of estrogen on cortisol binding globulin?

A

Decreases

5
Q

What is the most important amino acid in producing a glucogenic response?

A

Alanine***

6
Q

What is the effect of cortisol in the liver? Muscle? Adipose tissue?

A

Liver = glycogen synthesis

Other - glycogenolysis

7
Q

How does cortisol decrease the inflammatory response?

A

Inhibits phospholipase A2

8
Q

What are the three products of COX enzymes?

A
  • Prostacyclins
  • Prostaglandins
  • Thromboxanes
9
Q

What is the enzyme that produce leukotrienes? What is the substrate for this?

A

Lipoxygenase

Arachidonic acid

10
Q

Why may NSAIDs exacerbate asthma attacks?

A

Block COX will shunt to lipoxygenase pathway

11
Q

What nonsteroid hormone has intranuclear transduction?

A

Thyroxine

12
Q

What is the major hormone that is needed for neurological development in the newborn?

A

Thyroxine

13
Q

What is the most potent glucocorticoid?

A

Dexamethasone

14
Q

What is the most selective mineralocorticoid?

A

Fludrocortisone

15
Q

Why is it that low leads to lower insulin levels?

A

Lack of depolarization in the beta cells of the pancreas

16
Q

Why is it that cushing’s causes peptic ulcers?

A

Lower amounts of COX-1

17
Q

Why does Cushing’s cause myopathy?

A

Loss of muscle glycogen and protein d/t gluconeogenesis

18
Q

What are the three major drugs that inhibit the adrenal cortex?

A
  • Ketoconazole
  • Aminoglutethimide (aromatase inhibitor)
  • Spironolactone
19
Q

What is the MOA of ketoconazole in terms of adrenal function?

A

Inhibits desmolase

20
Q

What are the three major steroids that have mineralocorticoid effects?

A
  • Aldosterone
  • Fludrocortisone
  • Deoxycorticosterone
21
Q

What are the two major lethal side effects of corticosteroids?

A

CHF

Hypokalemia

22
Q

What is the major breakdown product of testosterone / estrogen, androsterone etc? When are these elevated?

A

Ketosteroids–Cushing’s, testicular CA, PCOS

23
Q

What is Cushing’s disease vs syndrome?

A

Disease is primary pituitary adenoma

Syndrome = 2/2 to some other cause

24
Q

Which is active: cortisol or cortisone?

A

Cortisol is active

25
Q

What is the function of HSD-1? HSD2?

A

HSD-2 is only in the nephrons, and inactivates cortisol, to prevent action on the mineralocorticoid receptors

26
Q

What is the issue with licorice?

A

Inhibits 11-HSB 2

27
Q

What happens to WBCs with cushing’s and addison’s?

A

Eosinophilia in addison’s

Eosinopenia in cushing’s

28
Q

What is the classic metabolic disturbance with Cushing’s?

A

Hypokalemic alkalosis

29
Q

What are the classic cancers that cause Cushing’s?

A
Thymomas
Oat cell CA
Pheo
Islet cell tumors
Carcinoid tumors

(TOPIC)

30
Q

What is Conn’s syndrome?

A

Adenoma or hyperplasia of the zona glomerulosa

31
Q

What are the cells that produce renin?

A

JG cells

32
Q

What does the macula densa sense, and do?

A

Senses renal flow, and will decrease JG cells from releasing Renin

33
Q

What are the two main immediate stimulants of aldosterone secretion?

A

Hyperkalemia and ANG II

34
Q

What happens to renin with CHF?

A

Increases

35
Q

What are the receptors on JG cells?

A

Beta 1 receptors

36
Q

How does hyperthyroidism cause HTN?

A

Y is a part of thyroid hormone, and will increase epi/NE synthesis. This activates Beta-1 Receptors on JG cells, and activates the RAAS

37
Q

What is Bartter’s syndrome?

A

Renal defect of Na reabsorption and aldosterone failure to reabsorb Na and renal resistance to ANG II

(acts just like spironolactone? diuretics)

Causes JG cell hyperplasia, but still no Na reabsorption

38
Q

Is there HTN or peripheral edema with Bartter’s syndrome?

A

Nah dawg

39
Q

What is Liddle syndrome?

A

AD defect of Na channels in the kidney, that usually presents with high ECF, low renin