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Pathophys 2, Midterm > Endocrino > Flashcards

Endocrino Flashcards

1
Q

what are the 4 classes of hormones?

A

Amine (norepinephrine)
peptide (ocytocin)
proteins
steroids (one)

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2
Q

what are the secretion patterns of hormones?

A

Circadian: cortisol peak a 6 am
Pulsatile: burst, break, burst, break
Substrate-dependent: secretion depends on something (insulin)

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3
Q

lipid solubles hormones:

A

protein bound, longer half-life
Uber ride to destination

thyroxine (amine) & streroids
cortisol, aldosterone, ADEK

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4
Q

water soluble:

A

free/unbound, easy travel, short half-life

proteins & amines
insulin, parathyroid, calcitonin, norepinephrine, FSH, LH

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5
Q

What is positive feedback loop?

A

more you make, more you make (snowball effect)

stops when explodes and no more energy

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6
Q

What is negative feedback ?

A

more you make –> less tyou make

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7
Q

Only ___ hormones can have a physiological effect

A

free and unbound

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8
Q

hormone receptors

A

no receptors, no message

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9
Q

Where is the receptor for fat soluble hormone?

A

inside cell

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10
Q

Where is the receptor for water soluble hormones?

A

cell membrane, because can’t diffuse in membrane

g-protein cascade –> 2nd messenger (CAMP) goes in cell

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11
Q

What is the water soluble response?

A
  1. non steroid hormone (1st messenger)
  2. g-protein coupled receptor
  3. ATP
  4. cAMP (2nd messenger)

regulate protein activity

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12
Q

What is the lipid-soluble response?

A
  1. bound to carrier-protein to travel in bloodstream
  2. steroid
  3. nucleus

regulates protein synthesis

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13
Q

What is ADH ?

A

regulated by osmoreceptors/baroreceptors, activates V2R at kidney tubular cells and increase water reabsorption

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14
Q

cortisol and T2DM

A

cortisol –> obesity, increase lypolyse and blood glucose –> increase free fatty aids –> insulin release –> insuline insensitivity –> B-cells destruction –> DB2 –> increase free fatty acids –> increase lipogenesis and blood glucose –> obesity

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15
Q

cortisol and female reproduction

A

stress –> CRH–> ACTH –> CORTISOL –> b-endorphins –> GnRH –> LH, FSH, Estradiol –> target tissue

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16
Q

types of stress

A 
conditioned response (pavlov)
anticipatory (exam)
reaction response ( adrenaline rush)
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17
Q

chronic stress

A

Th1 to Th2 –> immunosuppression

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18
Q

cortisol and immunity

A

inhibits Th1 –> immunosuppressant

19
Q

types of insufficient hormonal supply:

A

insufficient synthesis
feedback system failure
inactive hormones
delivery dysfunction

20
Q

types of inappropriate hormonal response:

A

cell receptor disorder

intracellular disorder

21
Q

what is SIADH

A

excessive ADH –> ++ H20 reabsorption –> increase ECF –> hyponatremia, hypoosmolarity

22
Q

sodium concentrations

A

normal : 145 mmol/l
thirst, fatigue, no edema : 140-130
120-130: severe GI distress
< 115 : confusion, seizures

23
Q

What is Diabetes insipidus (DI) ?

A

insufficient ADH –> increase diuresis –> polyuria, polydipsia(drinking) –> increase risk of dehydration, hypernatremia, hyperosmolarity

24
Q

Types of DI?

A

neurogenic
renal
dipsogenic

25
Q

hypopituitary:

A

hypothalamus dysfunction or lesion to pituitary

Sx when panhypopituitary (all hormones decreased)

26
Q

hyperpituitarism –> increase prolactin –> ?

A

prolactonoma:
- galaxrorrhea
- abnormal menses
- decrease estrogen
- hirsutism
- osteoporosis

  • small testies, erect dysfunction
27
Q

causes of hyperthyroidism :

A
  1. graves disease
  2. nodular goiter
  3. adenoma
  4. thyroid pill
28
Q

what is grave’s disease?

A

TSI immunoglobulines that act like TSH –> increase t3t4

s/c swelling, erythematous skin, exophthalmos
TSI intellect with ocular fibroblast receptors

29
Q

Causes of hypothyroidism:

A
  1. Hashimoto’s disease (autoimmune: TSI kill TH gland, less tissue, less synthesis)
  2. surgery/rx tx
  3. congenital
  4. iodine deficiency
30
Q

what is cretinism?

A

Hypo TH at birth

31
Q

Types of hyper PTH?

A
  1. Increase PTH and hypercalcemia : PT tumor
  2. Increase PTH and hypocalcemia : chronic kidney disease
  3. increase PTH and hypercalcemia (after an hypo) because system angry and takes all calcium from bones
32
Q

HypoPTH –> ?

A

hypocalcemia –> hyperphosphate –> less Vit D metabolize –> less Ca absorption

33
Q

What are the adrenocortical alterations?

A
  • Cushing’s disease
  • Hyperaldosteronism
  • Addison’s disease
  • Pheochromocytomas
34
Q

What is Cushing’s disease/syndrome

A

TOO much cortisol , no circadian rhythm

disease: internal environment (tumor) –>CRH –> increase ACTH –> increase cortisol
syndrome: exogenous cortisol (drugs)

acne, moon face, weight gain, more body hair

35
Q

cortisol –>

A

catabolic –> dumps all glucose in blood –> don’t need all –> stored as fat

36
Q

Consequences of hyper aldosterone

A

more NA reabsorption –>hyperNA –> more K excretion
hypoK –> polyuria, metabolize alkalosis, weakness, paralysis

hyperNA –> more plasma volume –> suppress renin-angio

1°: adrenal tumor
2°: extra-adrenal stimulus (more renin-angio 2)

37
Q

What is Addison’s disease ?

A

not enough cortisol

autoimmune destruction of adrenal cortex –> atrophy –> less cortisol

38
Q

What is pheochromocytoma?

A

adrenal medulla tumor –> more epinephrine

39
Q

What is T1DM?

A

cell mediated autoimmune destruction of beta-cells
insulin dependent (absolutely no secretion of insulin)
(no resistance to insulin)
prone to ketoacidosis
islet cells + insulin antibodies

40
Q

What is T2DM?

A 
insulin resistance (less insulin or more secretion) 
ketoacidosis only under stress 
no antibodies
41
Q

How to diagnose DM?

A
  • hemoglobine glyquée > 6.5 % (plasma glucose exposed to RBC)
  • fasting plasma glucose : > 7 mmol (126mg/dl) (100-125 more risk)
  • oral glucose tolerance testing : > 11. 1 (200) (75-99 more risk)
  • random glucose levels : 11. 1 (200)
42
Q

Metabolic syndrome criteria :

A

3 out of 5 :

  • increase waist circumference
  • plasma triglycérides > 150
  • low HDL
  • pre HT
  • fasting gluc > 100
43
Q

What is nephropathy?

A

increase renal BF –> increase protein excretion –” macro/microalbuminuria –> glomerular damage –> decrease glomerular filtration rate –> end stage kidney disease

44
Q

How does neuropathy occur?

A

Schwann cell injury, myelin degeneration., impaired nerve condition, impaired axonal transport and repair

  • -> neuropathy
  • -> demyelination and degeneration

Pathophys 2, Midterm (4 decks)

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