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Endocrinology > Pathophysiology 2 > Flashcards

Pathophysiology 2 Flashcards

1
Q

HTN increases the risk of?

A
  • stroke
  • heart failure
  • myocardial infarction
  • renal failure
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2
Q

Essential HTN?

A

95%

  • no underlying cause
  • treated to lower and reduce risk of other diseases
  • lifelong disorder requiring management
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3
Q

Secondary HTN?

A
  • 5%
  • diagnosable cause
  • can be cured by treatment of underlying cause
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4
Q

Symptoms of HTN?

A

-none except when super high

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5
Q

Prehypertension?

A

systolic 120-139
diastolic 80-89
-progress to HTN at rate of >10% per year
-lifestyle can reverse it back to normal

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6
Q

Renin-Angiotension-Aldosterone-System in Essential Hypertension

A

Low: better BP response to diuretics and CCB’s
Normal
High: CV risk, better to ACE inhibitors

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7
Q

Causes of Secondary HTN?

A
  • renal parenchymal disease (acute nephritis, chronic glomerulonephritis)
  • renovascular disease (renal artery stenosis, arteriosclerosis, fibroplasia)
  • endocrine causes
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8
Q

3 Endocrine Diseases that cause HTN?

A

-primary hyperaldosteronism
-pheochromocytoma
-Cushing’s syndrome
each less than 1%

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9
Q

Other endocrine conditions that cause HTN besides main 3?

A
  • acromegaly
  • diabetes mellitus
  • obesity
  • congenital adrenal hyperplasia
  • estrogen-induced hypertension
  • pregnancy-induced hypertension
  • renin-secreting tumors
  • hypothyroidism
  • hyperthyroidism
  • Liddle syndrome
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10
Q

Pheochromocytoma: Sympathochromaffin

A

1) sympathetic nervous system including postganglionic neurons, the vast majority of which release norepinephrine among other neurotransmitters
2) chromaffin tissues including particularly the adrenal medullae which are the major source of circulating epinephrine among other hormones

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11
Q

Norepinephrine & Epinephrine

A
  • catecholamines

- dihydroxyphenly nucleus and amine side chain

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12
Q

What comprises the autonomic nervous system?

A
  • sympathochromaffin system

- parasympathetic nervous system

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13
Q

Hemodynamic response to epinephrine?

A

-increased systolic, but not diastolic, BP and increased heat rate

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14
Q

Hemodynamic response to norepinephrine?

A

-increased systolic and diastolic BP with reflex restraint of the increased heart rate

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15
Q

Pheochromocytoma

A

-catecholamine producing tumors, composed of chromaffin cells, that typically produce labile hypertension and paroxysmal symptoms
Rare
1) HTN is curable
2) untreated risk for lethal THN paroxysm
3) some are malignant
4) clue to presence of familial AD syndrome

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16
Q

Pheochromocytoma Diagnosis

A

-clinical suspicion & biochemical confirmation and then anatomical localization

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17
Q

Pheochromocytoma Symptoms

A

-paroxysmal symptoms
-headache, diaphoresis, palpitations
-labile HTN
-family history
Precipitated by: positional changes, emotional stress, abdominal pressure, direct pressure on tumor, medications

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18
Q

Pheochromocytoma Metabolic Features

A
  • hypercatabolism

- increased metabolic rate, profuse sweating, hyperglycemia, weight loss

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19
Q

Pheochromocytoma Hematological Manifestations

A
  • orthostatic hypotension
  • elevated hemocrit
  • erythrocytosis INCREASED ERYTHROPOIETIN
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20
Q

Pheochromocytoma Biochemical

A

-measure metanephrines and and VMA
(metabolites)
-NE and E
-all measured in urine

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21
Q

Pheochromocytoma Location

A
  • in adrenal medulla 90%
  • 99% in abdomen
  • rest in mediastinum
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22
Q

Pheochromocytoma Treatment

A

surgical excision

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23
Q

Mineralocorticoid Excess

A

excess aldosterone

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24
Q

Mineralocorticoids

A
  • stimulate the distal renal tubules to reabsorb sodium from tubular fluid
  • excrete more potassium and hydrogen ions (acid)
  • increase open sodium and K+ channels in the luminal membrane of tubular cells and increase synthesis of basolateral membrane Na+/K+ ATPase, which generates the gradients that drive ion movement
  • expand extracellular fluid volume
  • increase blood pressure
  • lower plasma K+ levels, increase plasma pH 1
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25
Q

What activates the Mineralocorticoid Receptor?

A
  • cortisol

- aldosterone

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26
Q

Primary Mineralocorticoid?

A
  • aldosterone b/c an enzyme (11-beta hydroxysteroid dehydrogenase) coexists with this receptor in the renal tubule and converts cortisol to inactive cortisone
  • *Licorice make metabolite that inhibits 11-beta…**
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27
Q

Mineralocorticoid Excess causes?

A
  • HTN

- Hypokalemic alkalosis

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28
Q

What regulates Aldosterone secretion?

A

-volume of extracellular fluid

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29
Q

Dehydration Cascase

A

-Dehydration stimulates renin
-Renin causes release of angiotensin I, converted to angiotensin II by (ACE)
-ANG II stimulates aldosterone secretion
Negative Feedback Loop

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30
Q

Angiotensin II

A

potent vasoconstrictor

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31
Q

Renin secretion is stimulated by?

A

sympathetic nervous system (via beta-adrenergic receptors)

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32
Q

Is ACTH part of the physiologic control of aldosterone?

A

no

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33
Q

Mineralocorticoid Excess from?

A

1) autonomous aldosterone secretion
ex: adrenal adenoma (primary hyperaldosteronism)
2) increased renin secretion
(secondary hyperaldosteronism)

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34
Q

What is used to diagnose primary hyperaldosteronism?

A

-ration of plasma aldosterone to plasma renin activity

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35
Q

Primary Hyperaldosteronism

A

-excessive production of aldosterone due to adrenal disorder, NOT due to excess renin secretion

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36
Q

Secondary Hyperaldosteronism

A

-increased secretion of both renin and aldosterone

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37
Q

Etiology of Primary Hyperaldosteronism

A
  • 2/3 are do to aldosterone-secreting adrenal adenoma
  • small <2cm diameter
  • remaining of cases due to bilateral adrenal hyperplasia (idopathic)
38
Q

Clinical Findings of Primary Hyperaldosteronism

A
  • hypertension: increased Na+

- hypokalemia: may cause muscle weakness, cramps, polyuria

39
Q

Diagnosis of Primary Hyperaldosteronism

A

-suspected with hypertension & spontaneous hypokalemia
-excess aldosterone secretion is not under normal control by renin
ration of aldosterone/renin >50

40
Q

Glucocorticoids

A

-catabolic effects on protein metabolism
-suppress immunity & inflammation
-necessary for normal CV function
primary is cortisol
most commonly used drug: predisone
potent for negative feedback: dexamethasone

41
Q

Glucocorticoids Excess

A

Cushing’s Syndrome

  • obesity from appetite stimulation
  • catabolic effects cause weakness of skeletal muscle & connective tissue of skin
  • bone mass decreases & fractures common
  • 80% HTN by 1)angiotension 2)mineralocorticoid
    3) vascular reactivity
42
Q

Cortisol Angiotension in Cushings Syndrome

A
  • stimulate hepatic synthesis of angiotensinogen, acted upon by renin & angiotensin converting enzyme to the potent vasoconstrictor angiotension II
  • in some patients with Cushing’s
43
Q

Mineralocorticoid in Cushing’s Syndrome

A

-high conc. cortisol bind/activate mineralocorticoid receptors causing HTN and hypokalemia
-suppress plasma renin
cushings only with paraneoplastic production of ACTH

44
Q

Vascular reactivity in Cushing’s Syndrome

A

-give cortisol in normal subjects enhances vascular reactivity to pressors (causing vasocontriction), increased peripheral resistance and elevated BP

45
Q

What triggers realease of natriuretic peptides?

A

-increased wall stretch due to volume & pressure overload in patient with heart failure by atrial & ventricular myocytes

46
Q

Normal BNP

A

100 indicates heart failure also urine uroguanylin levels

47
Q

BMI

A

Weight (Kg)/ [Height (m)]^2

  • can overestimate degree of obesity in shorter muscular person
  • normal is 30 obese
48
Q

Total Energy Expenditure (TEE)

A

basal/resting energy expenditure (REE)*main
-decreases with age
thermic effect of food (TEF)
mandatory physical activities of daily living (ADL)
volitional physical activity or exercise
non-exercise activity thermogenesis (NEAT)

49
Q

non-exercise activity thermogenesis (NEAT)

A
  • activities of daily living

- yard work, walking to work, fidgeting

50
Q

What is the afferent limb of the energy homeostasis loop?

A

food consumption

51
Q

hunger is?

A

physiological response to appetite

52
Q

Arcuate Nucleus (ARC)

A
  • base of hypothalamus

- express hormone/neuropeptides that regulate feeding

53
Q

After eating, satiety signals are provided by?

A
  • vagal afferent projections to the brainstem

- GLP-1 and serotoninergic neurons

54
Q

Neuropeptide Y

A

-hypothalamic orexigenic signals
-rapidly stimulates food intake in rodents
hyperphagia and weight gain

55
Q

Agouti-related protein (AgRP)

A
  • hypothalamic orexigenic signals
  • expressed exclusively in arcuate nucleus of hypothalamus
  • increase food intake in rodents for several days (longer lived)
  • antagonism of melanocortin receptors MC3 & MC4
56
Q

Hypocretins/Orexins

A
  • hypothalamic orexigenic signals
  • stimulate food intake
  • hypo increase in response to exercise, neuroglycopenia & enforced wakefulness
  • hypo hormones localize to lateral hypothalamus
57
Q

Endocannabinoid System

A 
-endogenous signaling system 
receptors CB1 & CB2, endogenous anandamide
-activated to:
reduce pain/anxiety
modulate body temp. hormone release/smooth muscle tone
inhibit motor behavior
extinguish aversive memories
INDUCE APPETITE
58
Q

Overactivation of CB1

A
  • increase appetite by hypothalamus effect
  • increase motivation to eat effect nucleus accumbens
  • increase fat accumulation effect peripheral adipocytes
59
Q

Anorexigenic Neuropeptides

A
  • from hypothalamus inhibit food intake or induce satiety
  • melanocortins
  • cocain&amphetamine regulated transcript (CART)
  • serotonin
60
Q

Melanocortins

A
  • come from POMC
  • precurser that gives rise to ACTH, alphaMSH (act on MC receptors and decreases appetite)
  • weight loss = inhibition of POMC
61
Q

Leptin

A

-secreted by fat cells
-absence leads to overfeeding, massive obesity, delayed sexual maturation, immune defects in ob mice
Increased by feeding
Decreased during fasting, or after weight loss

62
Q

POMC/CART

A

-downstream effector neurons of leptin

63
Q

Serotonin

A
  • anorexigenic

- over ridden by SSRI’s

64
Q

Adiponectin

A
  • secreted in abundance by fat cells from insulin sensitive persons
  • deficient in persons with obesity/insulin resistance
65
Q

Insuline

A
  • regulate food intake through interaction with central hypothalamic neurons
  • secreted in direct proportion to fat mass
  • postprandial insulin secretion is potent signal for leptin secretion
66
Q

Pancreatic Polypeptide (PP)

A
  • secreted by specialized endocrine cells within islets of Langerhans
  • plasma levels increase after meal
67
Q

Ghrelin

A

-endogenous ligand for growth hormone secretagogue receptor
-synthesized/secreted by oxynic cells of stomach
(goes to anterior pituitary)
-stimulates growth hormone secretion by somatotrophs
-stimulates food intake
-peripheral signal for hunger & meal initiation

68
Q

Peptide YY

A
  • synthesized by mucosal endocrine L cells located in intestine and large bowel
  • released during feeding, serves as anorectic/satiety signal from intestinal cells
69
Q

Glucagon-like-peptide-1

A

-derived from precursor molecule preproglucagon
“incretins” - effect in boosting postprandial insulin secretion
-inhibition of feeding in rodents

70
Q

Cholecystokinin

A
  • best known for role in food digestion, stimulation of pancreatic enzyme secretion and gallbladder conc.
  • potent satiety factor
71
Q

Anorexigenic Signal of Leptin Targets?

A

Hypothalamus

72
Q

Anorexigenic Signal of Peptide YY Targets?

A

Hypothalamus

73
Q

Anorexigenic Signal of Pancreatic Polypeptide Targets?

A

Hypothalamus

74
Q

Anorexigenic Signal of Insulin Targets?

A

Hypothalamus

75
Q

Anorexigenic Signal of Cholecystokinin Targets?

A

Brain stem/ Vagus

76
Q

Anorexigenic Signal of GLP-1 Targets?

A

Local GI/diverse

77
Q

Orexigenic Signal of ghrelin Targets?

A

Hypothalamus

78
Q

What is the only food signal activated preprandially?

A

Ghrelin, the rest are activated by food ingestion and attenuated by fasting or starvation

79
Q

Causes of hypoglycemia?

A

1) iatrogenic

2) spontaneous

80
Q

Spontaneous Hypoglycemia?

A

1) fasting
2) postprandial
- nondiabetic populace

81
Q

Iatrogenic Hypoglycemia

A
  • hypoglycemia in the setting of diabetes
  • complicates therapy with insulin or sulfonylureas
  • limiting factor to aggressive efforts to achieve optimal glycemic control in patients with DM
  • Hypo is big problem with DM Type I
82
Q

Risk factors of Iatrogenic Hypoglycemia

A
  • skipped/insufficient meals
  • unaccustomed physical exertion
  • misguided therapy
  • alcohol
  • drug overdose
  • recurrent episodes of hypoglycemia
83
Q

Symptoms of Iatrogenic Hypoglycemia

A
  • Autonomic(neurogenic): tremulousness, sweating, palpitations, hunger b/c of increasing counterregulatory hormones - 1st
  • Neuroglycopenic: as glucose decreases further, impaired concentration, irritability, blurred vision, lethargy & development of seizure or coma - 2nd
  • Hypoglycemia unawareness: defective counterregulation, blunting of autonomic systems, seizures, coma without warning symptoms
84
Q

Isolated episodes of mild Iatrogenic hypoglycemia?

A

-may not require specific intervention

85
Q

Recurrent episodes of Iatrogenic hypoglycemia?

A
  • review lifestyle factors
  • content, timing, distribution of meals, meds dose and timing
    1) give readily absorbable carbs (sugar)
    2) IV dextrose for severe
    3) Glucagon if can’t maintain oral intake or no IV is avaliable
    4) Education
    5) Patients with hypoglycemia unawareness should monitor a lot
86
Q

Spontaneous Hypoglycemia

A

1) fasting

2) postprandial hypoglycemia

87
Q

Fasting Hypoglycemia

A
  • can be caused by inappropriate insulin secretion, alcohol, several hepatic/renal insufficiency, hypopituitarism, glucocorticoid deficiency
  • surreptitous insulin injection
  • ingestion of sulfonylurea
88
Q

Postprandial hypoglycemia

A

-suspect if vague symptoms hours after meal

89
Q

Alimentarly Hypoglycemia

A

-occur in patients with a history of partial gastrectomy or intestinal resection with symptoms 1-2 hrs after eating

90
Q

Functional Hypoglcemia

A

-symptoms of hypoglycemia (may or not confirmed by glucose measurement) occur in patients who have not undergone gastrointestinal surgery

91
Q

Diagnosis of Spontaneous Hypoglycemia

A

1) episodic autonomic symptoms
2) recurrent seizures, dementia, and bizarre behavior
3) definitive diagnosis
4) patients who develop hypoglycemia

Endocrinology (15 decks)

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