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Adv patho #4 > Endocrine System > Flashcards

Endocrine System Flashcards

1
Q

Insulin regulation

A
  1. Metabolic - ^ glucose and AA stimulates release
  2. Endocrine - stimulated indirec by GH and thyroxine
  3. Neural - enhanced by Para stim and inhibited by Symp stim
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2
Q

Insulin mech of action

A

Skeletal muscle, adipose tissue, and liver have insulin receptor cells.
1. Insulin binds to a subunits of ins receptor leading to autophos of b subunits > activate tyrosine kinase.

  1. Tyrosine Kinase activate pathways of intracellular signalling. (Pl3-K et MAP)
  2. Pl3-K - induces GLT-4 transporter to move to cell surfaced and transport glucose across membrane.Also mediates fat and protein metabolism.
  3. MAP - involved in mitogenic cell. activities
  4. Insulin not required for entry of glucose into tissues.
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3
Q

Insulin effect

A

Anabolic - building up from simple to complex substances

  1. Prevents breakdown and release of fuel.
  2. Inhibits catabolism
  3. Stimulates glycogen synthesis
  4. Promotes fat storage
  5. Stimulates lipogenesis
  6. Promotes protein synthesis.
  7. Inhibits gluconeogenesis.
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4
Q

Glucagon - regulations

A

Inhibited by ^ glucose, ^ insulin, ^ fatty acid, and ^ ketones.

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5
Q

Glucagon effect

A

Maintain glucose levels.

Stimulates breakdown of hepatic glycogen stores and hepatic glucose synthesis.

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6
Q

Somatostatin effect

A

Inhibits glucagon and insuline and its own secretion.

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7
Q
  1. Diabetes citeria
A

HYperglycemia d/t defects in insulin secretion or action or both.

DX:

  1. FBS > 126 more than once.
  2. S/S DM plus BS > 200
  3. BS >200 after oral glucose dose.
  4. (NEW) A1C >6.5
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8
Q
  1. Type I DM Epidemiology
A

Peak 11-13 yrs

Incidence has tripled.

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9
Q
  1. Type I DM Etiology
A
  1. Genetic susceptibility (fx hx, encodes Class II MHC molecules
  2. Environmental (prev infection or lack of )
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10
Q
  1. Type 1 DM Patho
A

Insulin deficiency caused by autoimmune destruction of pancreatic B cells.

  1. Cell mediated - failure of self tolerance of T cells (th 1 stimulate cytokines, th2 stimulate antibody secretion)
  2. Humoral - autoantibodies vs beta cells and insulin
  3. Inflammatory -
    a. macrophage activation > more b cell injury> insulitis
    b. mediates apoptosis
  4. Ongoing process leads to
    a. islet atrophy and fibrosis
    b. insulin deficiency
    c. 90% b cells depleted before S/S manifest.
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11
Q
  1. Type II Diabetes Epidemiology/Etiology
A

Occurs in adults, although growing juvenile subset.

Etio:
Genetic - defects in B cell function and insulin secretion

Environment -

a. physical inactivity
b. Diet
c. obesity

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12
Q
  1. Type II DM - Patho - Insulin Resistance
A

A. Peripheral tissue insulin resistance or respond to insulin.
Insulin resistance - largest contributor to DM.

  1. Insulin signalling pathway defects (# of receptors, def recep activity, MAP or Pl3-K or GLUT-4Trans problem)
  2. Obesity ( ^IC trig & ^free fatty acid met inhibit signalling. Fatty acid induce inflamm, adipokine problems, like leptin and adeponectin, are insulin sensitizing
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13
Q
  1. Type II DM Patho - Inadequate Insulin secretion
A

B. Inadequate Insulin Secretion

  1. B cell dysfunction > hypersecretion> hyperplasia
  2. B cell exhaustion > loss of pulsatile effect> hyposecretion.
  3. B cell failure
  4. B cell loss
    a. lipotoxicity> apoptosis.
    b. Glucotoxicity> hyperglycemia with excessive ROS injuring bcell. Islet cell do not produce much antioxidants.
    c. B cell loss by apoptosis, islet degeneration, deposition of amyloid. Basal level of ins produced but insuff to maintain normoglycemic > ceases.
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14
Q
  1. Gestational DM Epi/Etio
A

Emerges last half of pregnancy.

Risk Factors: Fx Hx, Obesity, older moms.

Dx : GTT

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15
Q
  1. Gestational DM Patho
A

GDM caused by:

a. insulin resist - hormones interfere with insulin action and receptor binding.
b. impaired secretion - may be d/t decrease bcell reserve

c. ^hepatic glucose production. - ^progesterone, cortisol, prolactin, and chorionic somatomam.
Stimulate glucogenolysis and gluconeogenesis.

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16
Q
  1. Diabetes - clinical manifestations
A
  1. Hyperglycemia -
    a. postprandial initially
    b. eventually fasting and pp
    c. glucosuria
    d. results in catabolic state
    e. glucagon, from alpha cells, stimulates glucosynthesis in liver
    e. ketosis from lypolysis d.t lipid catabolism
    f. ^ VLDL levels (d/t ^ fatty acids catabolism)
    g. negative nitrogen balance and muscle wasting by protein catbolism
  2. Polydypsia, polyuria (osmotic diuresis), polyphagia (hypothalamus satiety center activity decrease)
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17
Q
  1. Diabetes Complications - DKA
A

Occurs in Type I and II from not taking meds.

Predisp fx:

stressful situation such as infection, trauma, emotional stress by stimulates epi release and blocks residual insulin release and stimulates glucagon secretion.

Process in adipose tissue:

a. ^ lipolysis
b. free fatty acid uptake by liver
c. Hepatic mitochondria>aCoA> ketone bodies

Process in muscle:

a. AA release > ^Protein catab.
b. AA uptake by liver
c. FA and Ketoacids production

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18
Q
  1. Diabetic complications - DKA Clinical Manif
A

a. Severe hyperglycemia
b. ^serum osmolality from polyuria
c. ^ketone levels and ketonurea (metabolic acidosis, kussmauls, fruity breath)
d. Hyponatremia d/t diuresis
e. ^K (shift out of cell)
f. N/V, abd pain
g. coma (osmolality > 340mosm/L)

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19
Q
  1. Diabetic Complications - Hyperglycemic Hyperosmolar Non-Ketotic state
A

Occurs with Type II (esp elderly)

Charac by hyperglycemia (800-2400mgm/dl) and severe dehydration.

No ketoacidosis d/t sufficient insulin to prevent ketogenesis.

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20
Q
  1. Diab Complications - HHNK Clinical Manifestations
A
  1. Coma
  2. ^ glucose
  3. ^ serum osmolarity > 340
  4. life threatening
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21
Q
  1. Diabetic Complication - Hypoglycemia
A

Can occur secondary to diabetic treatment.

a. Insulin or oral antidiab meds.
b. Exercise- ^glucose uptake in muscle
c. Fasting - decreased glucose availability

Manifestations:

Shakiness, sweaty, palpitations initial s/s.

a. These result secondary to catecholamine release
b. nocturnal hypoglycemia if s/s occur at night, can lead to coma
c. CNS func alteration (neuroglycopenic) - confusion

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22
Q
  1. Chronic Diabetic complications
A

Overview - complications assoc with morb and mort in dm and occur 15-20 yrs into process.

Too much glucose for cell to use.

Excess glucose shunted along several pathways resulting in damage.

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23
Q
  1. Chronic Diabetic complications - AGE (advanced glycosylation end products)
A
  1. Glucose reacts with EC and IC proteins.
  2. Forms unstable intermediate (schiff base)
  3. Undergoes rearrangement to form stable intermediate.
  4. When occur with RBC > HgA1c
  5. With continued high glucose levels, stable interm further rearranges to an irreversible AGE product.
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24
Q
  1. AGE effects
A
  1. Inflamm d/t cytokine and growth factor release from macrophages
  2. ^ pro-coagulant activity
  3. ROS generation on endoth.
  4. Vasc. smooth muscle proliferation and EC matrix synthesis >thickening
  5. Abn crosslinking of EC matrix proteins > vasc stiffness and traps nonglycated plasma and interstitial proteins (ie ldl trapping>ateriosclerosis, also ^renal basement membrane thickening)
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25
Q
  1. Chronic Diabetic complications - Polyol Pathway
A
  1. Nerves, lenses, kidneys and blood vessels do not need glucose.
  2. Glucose converted to fructose by this pathway.
  3. Uses NADPH (cofactor enzyme req’d for glutathione antiox production).
  4. With ^ EC hyperglycemia > ^ IC glucose et depletes NADPH > dec glutathione >ROS injury
  5. Above tissues mainly affected.
26
Q
  1. Chronic Diabetic complications - Protein Kinase C pathway
A
  1. Protein C controls other proteins.
  2. ^ IC hyperglycemia stimulates more DAG formation>^protein kinase C production.
  3. Protein kinase C:
    a. ^prod of endo growth factor>neovascularization
    b. produces profibrinogenic molecules>^deposition of EC matrix and basement memb > thickening
    c. cytokine release > ROS injury > imparied NO production
27
Q
  1. Chronic Diabetic complications - Hexosamine Pathway (minor pathway for glycolysis)
A
  1. Turns off insulin signalling pathway > insulin resistance.
  2. Stimulates prod of transforming growth factor > microvascular damage
  3. ^release of cytokines> ROS damage
28
Q
  1. Chronic Diabetic Complications - Retinopathy
A
  • 49%
    1. Cap endo cell damage with BM thickening > macular edema and retinal ischemia
  1. Ischemia and Prot Kinase C > GF> neovascularization

Process:
1. Nonproliferative - vessel abn (^ tortuosity and dilation), microaneurysms, ^ vasc permeability (mac. edema).

  1. Preproliferative - cotton wool spots from infarcts
  2. Proliferative -
    neovascularizaton - angiogenesis (hemorrhage), retinal detachment, neovascular glaucoma
29
Q
  1. Chronic Diabetic complications - Nephropathy
A

35%
1. Epi - end stage more often in Type I, but more #s in Type II.
Common in native, african, mexican americans
2. Patho: AGE, sorbital(polyol), and protein kinase c.
3. Clinical manif:
microalbuminemia 30-300mgm/day to macroalbuminemia >300mg/day
M

30
Q
  1. Chronic Diabetic complications - Macro/microangiopathy
A

Macro - Premature atherosclerosis 43%
1. Commonly in Type II (60%deaths)

  1. ^ trig, VLDL, LDL in circ, ^ LDL trapping

MIcro: Diffuse thickening of BM by type IV collagen

31
Q
  1. Chronic Diabetic complications - HTN
A
  1. D/t alterations to fibrin, colagen, elastin in arteries secondary to AGE.
  2. Ros damage to endo cells (impairs NO formation, stimulates endothelin)
32
Q
  1. Chronic Diabetic complications - Diab neuropathy
A

40%
1. Excess glucose>pathway>ROS>neuronal injury impairing function in conduction and cell death.

  1. Injury secondary to microcirculation changes
  2. Occurs in peripheral nerves and autonomic nervous system.
33
Q
  1. Chronic Diabetic complications - Infection
A

D/t decreased:
1. leukocyte adherence
2. chemotaxis
3. phagocytosis
4. antioxidant activity
5. granulocyte (polymononuclear) function
Also, AGE alteration to circulating plasma proteins.

34
Q
  1. Hypothalamus - Hormones Secreted
A
  1. To the Posterior Pituitary - Oxytocin and ADH(vasopressin)
  2. To the Anterior Pituitiary
    a. CRH - stimulates ACTH
    b. TRH - stimulates TSH
    c. GnRH - stimulates LH and FSH
    d. GHRH - GH
    e. Prolactin Releasing Factor
    f. Growth Hormone Inhibiting Factor (Somatostatin )
    g. Prolactin Inhibiting Factor (dopamine)
35
Q
  1. Pituitary - Hormones Secreted
A
  1. Posterior Pit - Oxytocin, ADH
  2. Anterior Pituitary - secretory cells secrete 1 or more hormones.
    a. ACTH
    b. TSH
    c. Prolactin
    d. GnRH - LH/FSH
    e. MSH -Melanocyte SH (^ pigmentation - intermedia)
36
Q
  1. Hyperpituitarism -Anterior Pituitary
A

CX: ^ PH secretion

Etio:

a. Hyperplasia (intrinsic)
b. Adenoma (common- intrinsic)
c. Hypothalamus overproduction of RH (extrinsic)

Patho:

a. micro or macroadenoma
b. single cell type produces excess hormones
c. well circumscribed
d. classified on hormone they secrete (prolactin secreting adenoma most common)

Manif:

a. GH adenoma (gigantism before epiphysis closes, acromegaly when closed)
b. ACTH adenoma
c. Sella turcica abn.
d. visual abn (optic nerve compression)
e. ^ICP symptoms
f. endocrine abn

37
Q
  1. Hypopituitarism - Posterior Pituitaryw
A

CX: Decreased PH secretion

Etio:

a. Hypothalamus diseases, infection
b. Pituitary diseases
1. non-functioning pit. adenoma
2. Ischemic necrosis (Sheehan syndrome) loss of 75% ant pit gland cells
3. Infiltrative d/o
4. neoplasms(rare), radiation, sgy, genetic mutations

Clinical Manif:

a. Depends on the deficient hormone.
b. Adrenal insuff
c. Hypothryroidism
d. Amenorrhea/infertitlity
e. end-organ def. syndromes

38
Q
  1. Diabetes Insipidus - Posterior Pituitary Syndrome
A

Cx: polyuria

Etio:

  1. Central- ADH Def > loss of >85% of ADH secreting cells in hypo, d/t head trauma, tumor, inflam, sgy, edema
  2. Nephrogenic - renal tubule unresponsive to ADH
  3. Pregnancy - d/t ^ release vasopressinase

Clinic Manif:

  1. HyperNa
  2. ^ output
  3. Polydipsia
39
Q
  1. SIADH- syndrome of inappropriate of ADH secretion _ Posterior Pituitary
A

Cx: Excess ADh secretion

Etio: ectopic ADH secretion by malig neoplasms or hypo injury

Patho: Reasb of excessive amot of H2O

Clinic manif: hypoNa and neurologic dysfunc

40
Q
  1. Thyroid
A

Colloid contains stored thyroid hormones.

Regulation:

  1. TSH - thyrotropin - stimulates
    a. iodide uptake
    b. thyroglobulin synthesis
    c. T3/T4 secretion - quickly bound in serum and active portion is free. T4 prohormone for T3(^affinity for receptor sites).
  2. Inhibition - Negative Feedback Loop - by circulation T3/4 circulating inhibitng TSH or TRH.

Effects:

a. ^met. rate, heat prod, O2 consumption, bone/brain growth/development
b. ^CHO absorp, protein synthesis, lipid catabolism
c. Stimulates nervous system, hear rate and contractility.

41
Q

Calcitonin

A

Secreted by parafollicular cell or C-cells

  1. HyperCa stimulates release of calcitonin
  2. Inhibits osteoclastic bone reabsoption
42
Q
  1. Hyperthyroidism
A

Cx: ^ circulating T3/4

Etio:

  1. Graves disease
  2. Hyperfunctional multinodular goiter
  3. Hyperfunctional adenomas
  4. Exogenous thyroid intake
  5. TSH secreting pituitary adenoma (ext)

Clinical Manif:

  1. ^ T3/4 d/t pit aden or hypo diisease. (this time these do not inhibit tsh stimulation).
  2. ^ iodine uptake
  3. TSH-R(stim)Ab in Graves
  4. ^met rate, heat intol, wt loss, ^appetite.
  5. SNS overactivity ( ^CO, HR, tachy, poor concen, insomina, weakness, tremors), and altered skeletal system.
  6. ^ # and size of follicles, scanty colloid, lymphocytic infiltration
  7. Exophthalmosis ( infil of retro-ortbial space by leukocytes EC matrix, edema, rxn to TSHstim ab
  8. Thyroid storm - untreated thyrotoxicosis - tacy, fever, agitation, n/v, diarrhea, restlessness, psychosis.
43
Q
  1. Graves Disease
A

Autoimmune disorder

a. immune system attach self protein with lessened T cell tolerance
b. autoanitbodies to TSH receptor (Thyroid receptor stimulating ab)
c. Autoantibody activates TSH recep to ^ excess T3/4.

44
Q
  1. Hypothyroidism
A

Cx: TH def

Etio:

a. Hashimoto thyroditis
b. iodine def #1WW
c. thyroid ablation
d. fam/genetic mutation
e. drugs that inhibit release (lithium, amiodarone).

Clinic Manif:

  1. Low T3/4 levels
  2. ^ TSH
  3. Secondary hypoth - low t3/4
  4. ^ antibody titers in Hashimotos throiditis
  5. Decreased iodine uptake
  6. Cretinism (impaired dev of skeletal system, severe MR)
  7. Myxedema
    a. hypothermia, cold intol
    b. Dec metabolic rate, round puffy face, periorbital edema, wt gain, coarse hair
    c. muscle weakness
    d. slow thinking, depression
45
Q
  1. Hashimotos Thyroiditis (developed countries)****
A
  1. Breakdown in Tcell tolerance
  2. Autoab vs thyroid follicular cell membrane ( TSH-R(block) Ab)- tsh receptor blocking ab
  3. Autoab blocks recept stim of T3/4 prod.
  4. thyroid cell loss d/t CDt8 Tcell destruction, CD4th1 cytokine, ab cytotoxicity
  5. Leukocyte infil, follicular atrophy, gland fibrosis.
46
Q
  1. Goiters
A

Enlargement of thyroid gland - impaired synthesis of thyroid hormone (not related to receptor stimulation, tsh does bind to receptor)
Follicular cells are stimulated et develop hyperplasia.

Etio:

  1. dietary iodine def (most common)
  2. hypo or hyperthyroidism
  3. goitrogen ingestion
  4. enzymatic defects

Types:

  1. Diffuse nontoxic (simple) goiter
  2. Multinodular - d/t follicular cell response to ext stimuli
47
Q
  1. Parathyroid HOrmone
A

Chief cells secrete PTH.
Most calcium is in teeth and skeleton, rest is in ECF.

Regulation of PTH:

  1. Decreased Ca stimulates synthesis and secretion of PTH, and opposite.
  2. Phosphate levels also regulate but unknown.

Function:

  1. Regulates Calcium by
    a. stim Ca release from bone indirectly by osteoclast
    b. ^ reabsorp Ca
    c. Stim Vit D to active form
    d. ^ Ca absorp in gut
  2. Regulates phosphorus by ^ its excretion in kidneys
48
Q

Hypperparathyroidism

A

Excess PTH secretion
Etio:
a. para. adenomas or hyperplasia
b. neoplasia or carcinoma

Clinical manif:
a. ^ Ca and PTH levels
b. renal stones, bone fx, gi probs.
c. CNs disturbance, neuromusc abn
Ca important in membrane polarization.

Secondary parathy.
Cx: glandular hyperplasia / ^ PTH overproduction assoc with conditions that decrease Ca levels.

Etio:

a. renal failure (kidney not able to activate Vit d > Ca not absorb by intestine)
b. Vit D

49
Q

Hypoparathyroidism

A

Etio:

  1. sgy
  2. geneticmutations
  3. autoimmune loss

Clinic manif:

  1. hypoCa
  2. muscle spasms
  3. cardiac arryhtmias
50
Q
  1. Osteoporosis
A 
Increased porosity of skeleton from reduced bone mass.
Risk factors;
a. older age
b. white and asian
c. small boned
d. fam hx
e. sex hormone deficiency
f. smoking
g. low Ca/Vit D intake
h. sedentary lifestyle

Patho:
1. Decreased bone formation
2. Increased bone reabsorption
Result from imbalance in:
a. osteo blast/clast activity
b. osteoblast regulation of clast activation.
3. Bone loss mostly in abundant trabecular bone (wrist, spine, hip)
4. These are common fracture sites
5. Contributing factors:
a. estrogen def or dec testosterone (cytokine release, slow actvity)
b. age - Dec osteoblast replication or activity, slow Vit D prod, dec renal mass > dec Vit D activation, dec intestinal absorp of Ca.
c. Decreased ca and vit D intake stimulates bone reabsorption
d. Sedentary - increase reabsorp, dec remodeling, exceeds bone deposition
e. glucocorticoids dec osteoblast differentiation

Clinic Manif:

  1. Osteopenia density 1-2.5
  2. osteoporosis >2.5
  3. Frac of hip,spine, wrist
  4. Kyphosis
51
Q
  1. Hypercortisolism - (Exogenous) Iatrogenic Cushing Syndrome
A

Admininstration of exogenous glucocorticoids.

clinic manif:

a. hyposecretion of cortisol
b. z. fasciculata and recticularis atrophy
c. loss of normal response to stress

52
Q

Hypercortisolism - 70% (Endogenous) Primary Hypothalamic-Pituitary Cushing Syndrome or Cushing’s Disease

A

Etio:

a. ACTH hypersecretion
b. Ant pit ACTH-producing adenoma
c. Ant pit hyperplasia
d. Hypothalamic CRH tumor

Clinic manif:

a. ^cortisol levels
b. ^ ACTH levels

53
Q

Hypercortisolism - (Endogenous) Primary Adrenal Cushing Syndrome

A

Etio:

a. Adrenal gland function independent of ACTH
b. ^ cortisol secretion d/t adrenal adenomas or carcinomas
c. d/t cortical hyperplasia

Clinic manif:

a. ^ cortisol levels
b. low ACTH levels

54
Q

Hypercortisolism - 10% (Endogenous) Ectopic Cushing Syndrome

A

1, ACTH secretion by non-pit neoplasm.

2. Ectopic CRH causing ACTH secretion.

55
Q

Hypercortisolism - Clinical Manifestations M p 580

A

Due to the catabolic effects and symptoms of glucocorticoids.

a. Central obesity, buffalo hump, moon facies
b. Decreased muscle mass and weakness
c. Fragile, thin skin
d. Abdominal striae
e. Capillary fragility
f. Osteoporosis
g. HTN
h. ^ risk infections
i. neuropsych abn (depression, mood swings)
j. hirsutism, menstrual abn

Lab

a. ^ 24 urine cortisol level
b. loss of diurnal rhythym of secretions
c. hyperglycemia

56
Q
  1. Pheochromocytoma
A

Cx: neoplasms made of chromaffin cells and produce and secrete exccessive amt of catecholamines.

Etio:
a. Adrenal medulla neoplasm
10% malignant
b. familial genetic syndrome MEN2
c. chromaffin cell neoplasms in extramedullary sites

Clinic Manif:

a. HTN 90% of pts
b. Tachy, palpitations
c. HA, sweating tremors anxiety
d. N/V, wt loss
e. ^urinary excretion of free catech.

Complications:

a. cardiac issues - cardiomyopathy, ischemia, arrhythmias
b. pulm edema
c. renal artery stenosis

57
Q
  1. Hypoaldosteronism
A 
Cx: deficient mineralcorticoid production or action.
Etio:
Primary -
a. adrenocortical tissue destruction
b. defects in aldosterone synthesis
Secondary -
a. low renin production
b. hypopituitarism - inadeq stimulation of ald secretion

Clinic manif:

a. hypoNa
b. hypovolemia
c. hypotension
d. Impaired K secretion > hyperK
e. ^ renin levels with AC tissue destruction

58
Q
  1. Primary Acute Adrenocortical Insufficiency
A

Etio:

a. rapid w/d of long term med therapy
b. adrenal hemorrhage
c. stress from chronic AC insuff

59
Q
  1. Primary Chronic AC Insufficiency or Addison’s Disease
A

Etio:

a. Autoimmune destruction of adrenal cortex
b. Infections (tb,hiv)
c. Infiltrative diseases (amyloidosis, CA)

60
Q
  1. Clinical Manif of Primary AC Insufficiency
A

Deficiency of glucocorticoids and
mineralcorticoids (destruction of AC z.glomerulosa) :
a. hypovolemia
b. hypotension
c. lethargy and weakness
d. GI s/s: anorexia, N/V, wt loss
e. ^ ACTH>^melanocyte stim hormone > skin darkening

Lab:

a. hypoglycemia (impaired gluconeogenesis), hypoNa (aldos def)
b. ^K (inverse relationship with Na)
c. decreased cortical levels
d. ^ ACTH levels
e. inability of adrenal glands to produce cortisol in ACTH stimulation test.

61
Q
  1. Secondary AC Insufficiency
A

Etio:
Pituitary or hypothalamic hypofunction

Clinic Manif:

  1. Glucocorticoid deficiency
    a. decreased ACTH and endogenous cortisol levels
    b. hypothalamic hypofunction > decreasd CRH levels
  2. Androgen def
    a. male sex cx alterations
    b. decreased libido

Aldosterone remains normal.
No hyperpigmentation.

62
Q
  1. Hyperaldosteronism
A

Aldosterone excessive production

Etio:
Primary- autonomous overproduction of aldosterone.
a. AC adenoma (Conn Syndrome) or carcinoma
b. Z glomerulosa hyperplasia
c. genetic alterations that ^ aldosterone synthesis

Secondary
^ aldosterone secretion by renin-angiotensin overactivation

Clinic Manif:

a. HyperNa, Hypertension
b. HypoK
c. muscle weakness, cardiac dysrhthmias, visual disturbances

Lab:

a. primary - ^aldosterone levels and depressed renin levels
b. secondary - ^ aldosterone and renin levels

Adv patho #4 (2 decks)

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