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ENDO 207 FINAL > Actual PHYSIO > Flashcards

Actual PHYSIO Flashcards

1
Q

Give the manifestation of Panhypopituitarism

A

Sheehans and simmods

Decrease GH premature senility

Decrease thyroid function

Hypoglycemia

Sterility

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2
Q

Mentions the extrarenal effects of Vasopressin (ADH)

A

B– Extra-renal effects:

  1. In vascular system: Act on V1 receptors →↑ Ca2+ influx → VC →↑ ABP in hemorrhage (minor effect) RAAS & Sympathetic nervous systems are the primary regulators of ABP.
  2. In stress: ADH & CRH are co-secreted→ stimulates corticotropes → ↑ACTH →↑cortisol
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3
Q

11.Describe the cellular mechanism of action of thyroid hormones?

A

Regulate gene expression:

a. T3 (mainly) & T4 bind to ligand binding domain of receptor.

b. Hormone –Receptor complex stimulate DNA transcription →formation of mRNA → translation in ribosomes →formation of many proteins.

These proteins either:
* Directly: induce cellular functions, or
* Indirectly: bind to new gene→ formation of new proteins → powerful cellular functions

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4
Q

13.What are the effects of thyroid hormones on body metabolic processes?

A

A. On CHO metabolism:
* ↑glucose absorption, ↑insulin secretion, ↑glucose uptake by the cell,
* ↑ glycolysis & gluconeogenesis

B. On fat metabolism:
* ↑lipolysis→ ↑FFA oxidation
* ↓plasma cholesterol & ↑its secretion in bile via ↑LDL receptors on liver

C. On protein metabolism: anabolic

D. On BMR (40Calories / hr / m2 ) & normal body weight &appetite: necessary

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5
Q

16.Give an account on Regulation of Thyroid function?

A
  1. Hypothalamus: TRH →bind G proteins on anterior
    pituitary thyrotropes→ activates PLC → ↑intracellular Ca2+ → ↑TSH release
  2. TSH: binds G proteins receptors on thyroid cells → activation of ACE →↑cAMP → activates kinase → phosphorylation in thyroid cells

A. Within 30 min: ↑proteolysis of thyroglobulin→↑T3 &T4 in blood.

B. Within hours, days, and weeks:
* ↑size, number, secretory activity of thyroid cells.
* Activation of iodide pump
* ↑ Iodination of tyrosine & formation of thyroid hormones.

  1. Feedback of thyroid hormones: ↑T3 &T4 →↓TSH by direct effect on hypothalamus →↓TRH
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6
Q

What is cretinism? Give its manifestation

A

Caused by hypothyroidism in childhood

wide nasal bridge, enlarged lips, protruded tongue
mentally retarded
Dwarfism
Sterile

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7
Q

What is myxedema? Give its manifestation

A

Caused by hypothyroidism in adults

feeling cold
Husky voice
Depressed mental and sexual function

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8
Q

State the hormones that are secreted by the thyroid gland

A

T3 T4
Thryocalcitonin

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9
Q

What are the functions of the preoxidase enzyme?

A

oxidizes I- to I. It also binds I to the thyroglobulin to form MIT and DIT.

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10
Q

Thyroid decrease cholesterol by

A

Increase secretion of cholesterol in bile and stool

Increased number of lipoprotein receptors on liver cells which removes LDL from plasma

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11
Q

Give the mechanism of action of parathromone

A

PTH binds to Gs which activates adenyl cyclase

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12
Q

Actions of parathormone

A

On bone: A- Rapid phase: “osteolysis” Start in min, continues for hours

*↑ permeability of osteolytic membrane to Ca2+ from bone fluid.

  • ↑intracellular Ca2+are pumped into ECF by Calcium pump.

PTH stimulates osteoblasts production of IL-6 and RANKL →stimulates osteoclasts proliferation

2- On Kidneys
* ↓ PO4—reabsorption in PCT
* ↑Ca2+ reabsorption in DCT

3- On the intestine: →↑Ca2+ , phosphate absorption

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13
Q

Regulation of PTH secretion

A

Feedback of Plasma Ca+2: decrease plasma Ca causes high PTH secretion

Increase PO4 which decrease Ca+2 which causes PTH secretion

Vitamin D inhibits formation of PTH which causes decrease secretion

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14
Q

Hyperparathyroidism types

A

1ry: tumor of parathyroid

2ndary: hyperplasia of parathyroid glands in response to low calcium level

3rd: independent nodule secreting excessive parathyroid hormone after long period of 2ndary

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15
Q

Vitamin D3 origin and mechanism of action

A

in skin keratinocytes activated by sunlight

1,25(OH)2D3 binds to cytoplasmic receptor–> HR complex—> stimulates transcription —> formation of Calbindin D

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16
Q

What are the actions of Vitamin D3

A

On intestine: increase Calbindin D —> increase Ca transport from brush border to basolateral membrane

On bones: High Ca & PO4 —-> stimulates osteoblastic activity

On kidney: increase calbindin D —> increase Ca absorption by DCT

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17
Q

How is vitamin D3 regulated

A

Decrease plasma Ca+2 —> increase PTH —-> activate 1alpha hydroxylase –> increase 1,25 DHCC

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18
Q

Give the origin of Calcitonin and mechanism of action

A

Parafollicular cells of thyroid

Actions:

on bone: stimulates osteoblasts + decrease number and activity of osteoclasts + inactivate Ca+2 pump of osteocy

On kidney: increase Ca2+ and PO-4 excretion in urine

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19
Q

How is calcitonin secreted

A

increase plasma Ca+2

GIT hormones; to prevent hypercalcemia

Prolactin, dopamine and estrogen

20
Q

What is the effect of Glucocorticoids on metabolism

A

Carbs: stimulate gluconeogensis, glycogenesis. Decrease insulin sensitiviy by lowering affinity of insulin to receptors and decrease glucose transporter mobility

Protein: Catabolic

Fat: increase lipolysis –> FFA in plasma

21
Q

What are the effects of Glucocorticoids on body? CNS, CVS, Kidney, blood cells

A

CNS: modulates excitability and mood

CVS: maintain ABP by decreasing permeability of blood vessels

Kidney: increase GFR and blood flow. increase PO4 exceretion

RBC: increase platelets and RBC and decrease basophils

In stress: stress increases CRH –> increase ACTH–> increase cortisol

22
Q

What are some pharmacological effects of cortisol

A

On bone: osteoporosis due to decrease osteoblast and collagen formation

On CT: decrease collagen synthesis which makes skin and capillaries fragile

Anti inflammatory effect: blocks early stages of inflammation

Anti-Allergy: prevent histamine release

On immunity and lymphoid tissue: decrease cellular and humoral immunity

23
Q

Mechanism of action of glucocorticoid secretion

A

ACTH binds to G-protein receptor—> activates adenylyl cyclase —> increase cAMP which activates protein kinase A

24
Q

Give the cause of Cushing syndrome and give its manifestation

A

Adrenal tumor, bilateral hyperplasia of adrenal cortex

increase protein catabolism: Thin skin, poor wound healing, myopathy and osteoporosis

Fat metabolism: hyperlipemia and trunk obesity

Carbs: hyperglycemia and insulin resistant diabetes

Hirsutism due to androgen

25
Q

How does Aldosterone (mineralocorticoids) reabsorb Na?

A

Acts on DCT.

steroid hormone bind to cytoplasmic receptor—-> HR complex —> DNA transcription —> mRNA —> new proteins

This increase Na channels in luminal membrane

26
Q

Explain aldosterone regulation

A

Renin angiotensin system: angiotensinogen —-> angiotensin I. Then angiotensin I—> angiotensin II (by ACE)
renin: increase by hemorrhage, decreased by ANP

Plasma K is the most potent stimulant: increase of K stimulates aldosterone secretion by depolarizing adrenal cell –> open Ca—> stimulate aldosterone release

Plasma Na level: acute incline increase renin secretion. The decrease of ECF volume which increase aldosterone secretion.

27
Q

What is the cause of Addison’s syndrome? Give its effect

A

Hyposecretion of adrenocortical hormones

Glucocorticoid deficiency: decrease gluconeogenesis, muscle weakness, anorexia

Aldosterone deficiency: hyponatremia, polyuria, K retention

28
Q

Give the action of insulin

A

Carbs: hypoglycemic

On muscles: insulin binds to receptor –> movement of vesicles contain GLUT4 to membrane.–> increase glucose uptake by muscle

on liver: Insulin –> phosphorylation —> increase concentration gradient —> increase glucose uptake by liver

On Fat: decrease fat utilization. Increase lipogenesis

On protein: anabolic, increase transport of AA into cells

29
Q

Give the action of glucagon

A

Carbs: glycogenolysis, gluconeogenesis in liver

Fat: lipolysis

Protein: increase enzyme requirement

30
Q

Give the mechanism of action of glucagon

A

Glucagon binds with Gs receptor on liver cells —> activate ACE —> increase cAMP–> increase phosphorylase–> increase glycogenolysis

31
Q

Explain relation of insulin to potassium

A

Insulin –> activity of Na/K which increase k entry.

Infusion of insulin and glucose —-> temporary K in hyperkalemic patient with renal failure

32
Q

Give the control of secretion of insulin

A

Hyperglycemia (most potent) stimulus

Protein meals and AA

Glucagon secretion increase insulin

Oral glucose increase secretion

33
Q

Give the control of glucagon secretion

A

Hypoglycemia: increase glucagon as during starvation

Hyperglycemia

High protein meal: increase glucagon to balance insulin effect

Insulin: decrease glucagon secretion

CCK, gastrin: increase glucagon

34
Q

Give the regulation of secretion of somatostatin and give action

A

increase blood glucose, AA and FA
Increase GIT hormones as CCK

Action: prevent rapid turnover of food in git

35
Q
  1. Clarify the factors that regulate ovarian cycle.
A

A- Hypothalamus:

Secretes (GnRH). released at hourly rhythmic GnRH pulses and initiates the follicular phase, whereas the monthly rhythm of GnRH secretion produces the midcycle LH surge

During the first half of the ovarian cycle:

Negative feedback:
o ↑estrogen in the first week inhibit GnRH
o 1ry follicle containing high number of FSH receptors continues to respond to low level of FSH and becomes mature Graafian follicle

Positive feedback:
o Maintained high level of estrogen ((48 hrs) pre-ovulatory directly stimulate release of GnRH and produce mid cycle LH surge
o Activins, produced from granulosa cells during folliculogenesis, stimulate FSH and stimulates androgen synthesis and estrogen formation.

During the second half of the ovarian cycle:

Negative feedback:
o Estrogen + progesterone à inhibit production of FSH & LH
o Inhibin: inhibits FSH & ↓ estrogen formation

36
Q
  1. Explain the peaks of estrogen production during ovarian cycle
A

Preovulatory peak from graafian follicle (for LH surge and ovulation)

Midluteal peak from corpus luteum (smaller but longer)

37
Q
  1. Explain the effects of Estrogens on Cardiovascular System
A
  1. VD by local production of nitric oxide.
  2. Open K+ channels in the vascular smooth muscles.
  3. ↑ endothelial permeability to LDL thus inhibiting atherosclerosis–>↓ MI
  4. ↑ HDL and ↓ LDL formation.
  5. Antioxidant
38
Q
  1. Clarify in details actions of progesterone
A

1) On primary sex organ (ovaries): progesterone inhibit follicular growth

2) On secondary Sex Organs:

a. Fallopian Tubes: stimulates mucus secretion for nutrition of fertilized ovum.
b. Uterus: Controls secretory phase
c. Cervix: stimulate secretion of thick, mucus plug
d. Vagina: thick vaginal secretion and increase leukocytic infiltration.
e. Mammary glands: growth of lobule & alveoli

3) Thermogenic Effect: body temperature ↑ (0.5 C)

4) Respiration: stimulates respiratory center

5) Electrolyte balance: excess progesterone: stimulate Na, H2O retention

6) Effects on CNS: exerts brain-protective effects by protecting and rebuilding BBB

39
Q
  1. Clarify in details actions of estrogen.
A

1) On Primary sex organs (ovaries) Growth of ovarian follicles + Stimulate LH surge

2) On Secondary Sex Organs:
- Fallopian Tubes: ↑ number, motility of cilia
- Endometrium: stimulate proliferative phase.
- Cervix: stimulate secretion of thin alkaline mucus
- Vagina: Maintenance of epithelium to resist infections and trauma
- Mammary Glands: fat Deposition, pigmentation of areola+ Growth of ducts + Inhibits effect of prolactin.

3) Effects on Secondary sex Characters:
- Body configuration: Narrow shoulders, wide pelvis + Fat distribution in breast, buttocks
- Hair: Less body hair and more scalp hair
- Triangular public hair + Growth of pubic and axillary hair is due to adrenal androgens.
- Voice: high pitched child voice as estrogens do not stimulate growth of vocal cords

4) On bones : conserves the bone mass + anabolic effect + osteoblastic activity, union of epiphyses.

40
Q

Enumerate the causes and characters of anovulatory cycle

A

Causes:

o Insufficient LH surge.
o Failure of ovary to respond to LH.
o Excess prolactin or emotional stress.
o It Is normally present in First few cycles at puberty, Late cycles prior to menopause & lactation.

Characters:
* No corpus luteum—> no progesterone–> Absence of the secretory changes in endometrium.
* Cycles are short.

41
Q

Describe the endocrinal functions of placenta

A

HCG: Growth of corpus luteum, Growth factor for endometrium, Implantation & invasion of fertilized ovum.

HCS: growth of breast, provides glucose from mother to fetus

Estriol: growth of uterus, relaxation of pelvic ligaments, increase oxytocin receptors

Progesterone: uterine contractility, forms thick mucus plug, inhibit actions of prolactin and increase breast alveoli

Relaxin: relax pelvic ligament, softening of cervix, inhibition of uterine contraction

42
Q

Describe theories of labor

A

Hormonal factors: progesterone/estrogen ratio at 7th month were estrogen increase while progesterone doesn’t. Fetal oxytocin initiates labor. Cortisol causes uterine contractions

Mechanical factors:

  1. stretch of uterine muscles induces contractions.
  2. cervical stretch stimulates reflex uterine contractions.
  3. Positive Feedback theory of labor:
    Once the uterine contractions become greater than a critical level,
    a positive feed-back initiates a vicious circle of stronger contractions.
  • Cervical stretch by baby’s head—> cause reflex contractions in the body of uterus–> more cervical stretch and dilatation.
43
Q

Give an account on the uterine cycle

A

Estrogenic phase: day 5-14. Growth and proliferation of endometrium and its glands, Growth of its new blood vessels. Expression of progesterone receptors in endometrium

Progestational phase: day 14-menstral phase. Preparing endometrium for implantation of ovum. Increase of endometrial glands. Tortuous endometrial vessels

Menstrual phase: first 5 days. Sudden drop of estrogen & progesterone. VC of endometrial vessels which causes ischemia & necrosis of endometrium. death of blood vessels and rush of blood, Only deep thin layer of endometrium remain regeneration.

44
Q

Factors affecting spermatogenesis

A

LH: produce androgen on Leydig cells

FSH: promotes late stages of spermatid maturation

Androgen acting on Sertoli cells

Cretinism: impairs spermatogenesis

Temperature: need 32 C

45
Q

Give an account of puberty

A

Thelarche: development of breasts
Pubarche: development of axillary and pubic hair
Menarche: 1st menstrual cycle
Growth spurt
Adrenarche : secretion of androgen

ENDO 207 FINAL (4 decks)

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