Actual PHYSIO Flashcards
Give the manifestation of Panhypopituitarism
Sheehans and simmods
Decrease GH premature senility
Decrease thyroid function
Hypoglycemia
Sterility
Mentions the extrarenal effects of Vasopressin (ADH)
B– Extra-renal effects:
- 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.
- In stress: ADH & CRH are co-secreted→ stimulates corticotropes → ↑ACTH →↑cortisol
11.Describe the cellular mechanism of action of thyroid hormones?
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
13.What are the effects of thyroid hormones on body metabolic processes?
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
16.Give an account on Regulation of Thyroid function?
- Hypothalamus: TRH →bind G proteins on anterior
pituitary thyrotropes→ activates PLC → ↑intracellular Ca2+ → ↑TSH release - 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.
- Feedback of thyroid hormones: ↑T3 &T4 →↓TSH by direct effect on hypothalamus →↓TRH
What is cretinism? Give its manifestation
Caused by hypothyroidism in childhood
wide nasal bridge, enlarged lips, protruded tongue
mentally retarded
Dwarfism
Sterile
What is myxedema? Give its manifestation
Caused by hypothyroidism in adults
feeling cold
Husky voice
Depressed mental and sexual function
State the hormones that are secreted by the thyroid gland
T3 T4
Thryocalcitonin
What are the functions of the preoxidase enzyme?
oxidizes I- to I. It also binds I to the thyroglobulin to form MIT and DIT.
Thyroid decrease cholesterol by
Increase secretion of cholesterol in bile and stool
Increased number of lipoprotein receptors on liver cells which removes LDL from plasma
Give the mechanism of action of parathromone
PTH binds to Gs which activates adenyl cyclase
Actions of parathormone
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
Regulation of PTH secretion
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
Hyperparathyroidism types
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
Vitamin D3 origin and mechanism of action
in skin keratinocytes activated by sunlight
1,25(OH)2D3 binds to cytoplasmic receptor–> HR complex—> stimulates transcription —> formation of Calbindin D
What are the actions of Vitamin D3
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
How is vitamin D3 regulated
Decrease plasma Ca+2 —> increase PTH —-> activate 1alpha hydroxylase –> increase 1,25 DHCC
Give the origin of Calcitonin and mechanism of action
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
How is calcitonin secreted
increase plasma Ca+2
GIT hormones; to prevent hypercalcemia
Prolactin, dopamine and estrogen
What is the effect of Glucocorticoids on metabolism
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
What are the effects of Glucocorticoids on body? CNS, CVS, Kidney, blood cells
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
What are some pharmacological effects of cortisol
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
Mechanism of action of glucocorticoid secretion
ACTH binds to G-protein receptor—> activates adenylyl cyclase —> increase cAMP which activates protein kinase A
Give the cause of Cushing syndrome and give its manifestation
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
How does Aldosterone (mineralocorticoids) reabsorb Na?
Acts on DCT.
steroid hormone bind to cytoplasmic receptor—-> HR complex —> DNA transcription —> mRNA —> new proteins
This increase Na channels in luminal membrane
Explain aldosterone regulation
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.
What is the cause of Addison’s syndrome? Give its effect
Hyposecretion of adrenocortical hormones
Glucocorticoid deficiency: decrease gluconeogenesis, muscle weakness, anorexia
Aldosterone deficiency: hyponatremia, polyuria, K retention
Give the action of insulin
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
Give the action of glucagon
Carbs: glycogenolysis, gluconeogenesis in liver
Fat: lipolysis
Protein: increase enzyme requirement
Give the mechanism of action of glucagon
Glucagon binds with Gs receptor on liver cells —> activate ACE —> increase cAMP–> increase phosphorylase–> increase glycogenolysis
Explain relation of insulin to potassium
Insulin –> activity of Na/K which increase k entry.
Infusion of insulin and glucose —-> temporary K in hyperkalemic patient with renal failure
Give the control of secretion of insulin
Hyperglycemia (most potent) stimulus
Protein meals and AA
Glucagon secretion increase insulin
Oral glucose increase secretion
Give the control of glucagon secretion
Hypoglycemia: increase glucagon as during starvation
Hyperglycemia
High protein meal: increase glucagon to balance insulin effect
Insulin: decrease glucagon secretion
CCK, gastrin: increase glucagon
Give the regulation of secretion of somatostatin and give action
increase blood glucose, AA and FA
Increase GIT hormones as CCK
Action: prevent rapid turnover of food in git
- Clarify the factors that regulate ovarian cycle.
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
- Explain the peaks of estrogen production during ovarian cycle
Preovulatory peak from graafian follicle (for LH surge and ovulation)
Midluteal peak from corpus luteum (smaller but longer)
- Explain the effects of Estrogens on Cardiovascular System
- VD by local production of nitric oxide.
- Open K+ channels in the vascular smooth muscles.
- ↑ endothelial permeability to LDL thus inhibiting atherosclerosis–>↓ MI
- ↑ HDL and ↓ LDL formation.
- Antioxidant
- Clarify in details actions of progesterone
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
- Clarify in details actions of estrogen.
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.
Enumerate the causes and characters of anovulatory cycle
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.
Describe the endocrinal functions of placenta
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
Describe theories of labor
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:
- stretch of uterine muscles induces contractions.
- cervical stretch stimulates reflex uterine contractions.
- 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.
Give an account on the uterine cycle
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.
Factors affecting spermatogenesis
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
Give an account of puberty
Thelarche: development of breasts
Pubarche: development of axillary and pubic hair
Menarche: 1st menstrual cycle
Growth spurt
Adrenarche : secretion of androgen
