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IP week 13 endocrine > Adrenal Patho And Physio > Flashcards

Adrenal Patho And Physio Flashcards

1
Q

Addison’s disease Definition and symptoms

A

Adrenal insufficiency / failure to produce hormones

Weight loss-not for diagnosis

Fatigue

Weakness

Dizziness upon standing

Abdominal pain

Suspended menstrual cycles

Dehydration

Increased potassium in blood

Decreased sodium in blood

Low BP

Skin discoloration

Depression

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2
Q

Cushing’s syndrome Definition and symptoms

A

Hyperadrenocorticism

Weight gain

Lipodystrophy-buffalo hump

Moon face/temporal filling

Dial action of capillaries-telengiectasis- stretch marks

Excessive sweating-hyperhidrosis

Hirsutism

Low libido

Impotence

Amenorrhea/Infertile

Polyuria/dipsia

Hypokalemia

High BP

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3
Q

2 types of glucocorticoids

A

Cortisol

Corticosterone

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4
Q

1 type Mineralcorticoid and origin

A

Aldosterone From zona glomerulosa

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5
Q

1 type androgen

A

Androstenedione

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6
Q

Aldosterone description and what happens in absencence

A

Required for reabsorbtion of Na in exchange for K

In absence plasma K inc. (arrhythmia)

Plasma Na and Cl dec.

Dec. volume

Dec. CO

RESULTS IN SHOCK/ HYPOTENSION/ DEATH in 2 weeks

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7
Q

MOA Aldosterone

A

Diffused into tubular cells Bind to proteins Hormone-receptor complex enters nucleus to make mRNA of sodium channels and Na-k ATPase

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8
Q

How to increase aldosterone. 6 ways

A

High K in ECG

Dec BP

Dec. blood volume

RAAS

Low Na

ACTH-pituitary hormone

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9
Q

Glucocorticoids definition and MOA and origin

A

Hormones are responsible for RESPONDING TO STRESS

MOA: similar to aldosterone but results in metabolism

* cortisol produces faster effect

Decrease BG/ muscle weakness

Susceptible to stress-death

From zona fasciculata

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10
Q

Glucocorticoids in glucose metabolism

A

Increase: gluconeogenesis/ glycogen synthesis in liver

Decrease: Glycolysis/ glucose transport into cells Effect:increase blood glucose (adrenal DM)

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11
Q

Glucocorticoids in liver metabolism

A

Increase: movement of fat FROM adipose tissue / plasma FFA/oxidation of FA

increase hepatic glucose PRODUCTION by inc. substrate availability via proteolysis and lipolysis

****induce hyperinsulemia and insulin resistance, tx as DM2

Decrease: glucose used in adipocytes/TG synthesis

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12
Q

Glucocorticoids in protein metabolism

A

Increase: catabolism

Decrease: stores in all tissues EXCEPT liver/ synthesis/ AA transport into extra patio tissues/ formation of RNA in extraheoatic tissues In liver: increase AA transport/ synthesis/ plasma proteins/ gluconeogenesis

Effect: transfer of AA FROM MUSCLE TO LIVER

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13
Q

Inflammatory pathway

A

Increase cell damage

Histamine cause vasodilation Increase capillary permeability

Increase infiltration of leukocytes

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14
Q

Glucocorticoids and inflammation intervention

A

Increased stabilization of lysosomal membrane = decrease release of enzymes

Cortisol dec. vasodilation

Cortisol decrease capillary permeability

Cortisol dec. migration of leukocytes

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15
Q

Cortisol secretion

A
  1. CRH
  2. ACTH
  3. Cortisol
  4. inhibits
  5. Stimulate
  6. Promote
  7. Inhibit
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16
Q

ACTH function/ origin

A

Adrenocorticotrophic hormone Stimulated by CRH From hypothalamus Released from anterior pituitary

Causes: Cortisol secretion from adrenal cortex (zone fasciculata) Aldosterone secretion from adrenal cortex (zone glomerulosa) Bind to melanocytes to increase melanin

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17
Q

Androgens definition and origin

A

Weak androgens secreted then converted to testosterone by peripheral tissues. Stimulate pubic and axillary hair growth and sexual drive in females

From zona reticularis

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18
Q

Adrenal Medulla Hormones and function

A

Epinephrine: Increase blood glucose Increase fat breakdown in fat tissues Dilation of bv in skeletal muscle and cardiac muscle

Epi and NE: Inc. HR and force BV constriction in skin/ kidneys/ GI

19
Q

Diagnosis of low aldosterone secretion

A

EKG: T wave is high from K Blood work for aldosterone

20
Q

Diagnosis of low glucocorticoids

A

Blood cortisol levels

Increased ACTH

21
Q

3 Addisons causes

A

Autoimmune response against cortical tissue

Bacterial infection

Cancer

22
Q

Addison’s diagnosis and treatment

A

Dianosis: Measure ACTH will be high

Inject or with 250mcg corticotropin (ACTH) if no rise in cortisol positive diagnosis normal rise is >20mcg/dl

Treatment: Aldosterone injection AND Glucocorticoid injection or oral

Hydrocortisone 300mg IV daily & taper to LIFELONG maintenance dose of 15-20mg AM 5mg PM

2/3 dose in AM 1/3 dose PM (stimulate circadian G production)

Fludricortisone 0.1mg daily

23
Q

3 causes of Cushing’s disease and effects

A

Hyperplasia of adrenal corticies (increased ACTH)

Increased cortisol from tumer

Hyperplasia of adrenal corticies in non- pituitary tissues

Brackett’s reasons

systemic inflammatory diseases

solid organ transplant

cancer

steroid administration

Effects: Increased androgens- hair and infertility in women Increased fat movement- buffalo hump Increased BP- b/c mineralcorticoid activity Increased glucose, Increased protein catabolism-muscle-weakness/ low immunity/ osteoporosis

24
Q

Diagnosis of Cushing’s

A

Diagnosis:

  • Measure plasma cortisol will be high
    • normal serum cortisol
    • 16-20 mcg/dl in AM
    • 6-10 mcg/dl
  • Dexamethasone suppression test
  • increased ACTH
    • normal <80

LDT: 1 mg dexamethasone/ no change in cortisol is abnormal = cushing’s

HDT: 8mg dexamethasone

  • less cortisol cushing’s is from pituitaty ACTH producing tumor
  • no change in cortisol cushing’s is from adrenal tumor or ectopic ACTH producing tumor
25
Q

Primary aldosteronism definition and treatment

A

Small tumor in cells which produce aldosterone Low K ,HTN ,Glucocorticoids normal

Treatment: remove tumor

26
Q

Adrenogenital syndrome defintion and treatment

A

Inherited disorder of adrenal gland due to lack of enzyme 21-hydeoxylase Tumor secretes androgens Intense masculinization Tumor hard to detect in men

Treatment: Dexamethasone/fludrocortisone/hydrocortisone

27
Q

Treatment of Cushing’s

A

corrective intervention (surgery) if possible

manage signs and symptoms

28
Q

What to Manage in G excess/Cushing’s s/s

A

decrease cortisol

glucose control

mood stabilizaiton

HTN control

Protect against osteoporosis

29
Q

Ketaconazole in G

moa and dose

A

manages excess G (cushing’s)

inhibits 1st step in cortisol sysnthesis, and the conversion of 11-deoxycortisol to cortisol

potent inhibit of c17-20 desmolase (decrease androstenedione and testosterone)

Dose: 200mg 2-3qd

30
Q

how much cortisol do the adrenal glands produce

A

15-30mg daily

31
Q

G comparison of doses

hydrocortisone

prednisone

methylprednisolone

dexamethasone

A

Hydrocortisone

  • 20mg
  • no G high M

prednisone

  • 5mg
  • some G and M

Methylprednisolone

  • 4mg
  • some G and no M

Dexamethasone

  • 0.75mg
  • high G no M
32
Q

Prevention or Minimization of Iatrogenic G excess

A

minimize dose and length of tx

use of steroid-sparing therapies

dose steroids in AM b/c cortisol highest in AM from GH overnight

use lowest dose

QOD if possible

33
Q

Purpose of FRAX tool

A

assessment of fracure risk

34
Q

NNT

A

numer needed to treat

average number of patients who need to be treated to prevent one additional bad outcome

1/ARR (absolute risk reduction)

35
Q

Primary Adrenal insufficiency

A

failure of adrenal gland itself

destruction of adrenal cortex either rapidly or slowly, and loss of BOTH G and M

Acute: sepsis/adrenal hemorrhage

  • ab. pain/fever/chills/HA/hypotension/death

Chronic: Addison’s/HIV/TB

  • weak/weight loss/ hypotension/ hypoglycemia/ hyperpigmentation
36
Q

secondary adrenal insufficiency

A

failure of hormone production

failure of piuitary/hypothalamus

suppression of adrenal function by steroids

37
Q

G overtreatment

A

weight gain

adnormal fat distribution

osteopenia

hyperglycemia

38
Q

G undertreatment

A

myalgias

Flu-like

anorexia

GI upset

fever

hypoglycemia

39
Q

M overtreatment

A

HTN

low plasma renin

low K (great way to measure it)

possibly high NA

40
Q

M undertreatment

A

orthstatsis(SBP drop 20, DBP drop 10, HR inc. 20)

Fatigue

inc. plasma renin

inc. K
possibly low Na

41
Q

M and G in physiologic stress

A

minor: DOUBLE G daily until better
major: 150-300mg HC

42
Q

HPA axis

A

G dose <10-14 days will not change it

use cosyntropin stimulation test for HPA axis suppression

HPA will recover after 1 month for ACTH, and 2-3 months for cortisol, 1 year for stress response

43
Q

do steroids suppress fever?

A

YAS

44
Q

Pneumocystis jeroveci pneumonia prophylaxis

A

cause: prednisone >10mg/day

Tx: bactrim 1qdx21d

IP week 13 endocrine (8 decks)

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