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Medicine 1 VCS860 > HYPERadrenocorticism > Flashcards

HYPERadrenocorticism Flashcards

1
Q

Adrenal Gland Physiology

Medulla

A

central core

a sympathetic ganglion that has lost its axon

Produces norepinephrine, epinephrine and dopamine

Composes 28% of the entire adrenal mass

Cat - secretes primarily norepinephrine: Dog - Primarily Epinephrine

Actions of Hormones

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2
Q

Adrenal Gland Physiology

Cortex

Zona Glomerulosa

A

outer most layer

mineralocorticoids - aldosterone

the cells of this layer can regenerate the other two layers

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3
Q

Adrenal Gland Physiology

Cortex

Zona Fasciculata

A

Glucocorticoids - cortisol

Largest of the 3 zones

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4
Q

Adrenal Gland Physiology

Cortex

Zona Reticularis

A

inner most layer

Sex steroids

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5
Q

Adrenal Gland Physiology

Hormone Production

A

All hormones of the adrenal cortex are derivatives of cholesterol

Cholesterole ester hydrolase liberates cholesterol

Cholesterol transported to the mitochondria and converted by cholesterol desmolase to pregenolone

Pregenolone is transported to the SER, converted to progesterone and 17-hydroxyprenenolone

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6
Q

Adrenal Gland Physiology

Hormone Release

Corticotropin-Releasing Hormone

A

Released by hypothalamus

Provides control over secretion of adrenocorticotropin hormone release from pituitary

CRH - release influenced by

set-point/basal release

diurnal rhythms

Input from nociceptive pathways

Input from limbic system during stress

Hypoglycemia

Cortisol-negative feed back on release

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7
Q

Adrenal Gland Physiology

Hormone release

Adrenocorticotropic Hormone (ACTH)

A

Produced from corticotrophs in the pituitary gland

ACTH serum half life : 10 minutes

Function: Stimulate cortisol release from adrenal cortex,

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8
Q

Adrenal Gland Physiology

Glucocorticoids

A

Cortisol - Zona fasciculata but also zona reticularis

Physiological effects

Metabolism

Gluconeogenesis/glycogeneisis

protein catabolism

Lipolysis

Antagonizes the effect of insulin

Anti-inflammatory / immunosuppressive effects

Modulate function of many cells: bone marrow, GI mucosal barriers, Renal calcium excretion, others

Regulation of Cortisol Secretion:

CRH and ACTH secreted in a pulatile manner

ACTH secretion increases in response to feeding:

Stress

pain

trauma

pyrogens

cold exposure

Surgery

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9
Q

Adrenal Gland Physiology

Mineralocorticoids

A
  • Aldosterone - Zona glomerulosa
  • Physiologic effect: sodium, potassium, and water homeostasis
  • Regulation of aldosterone secretion:
    • Primary controls:
      • Serum potassium levels
      • Renin-angiotensin system
    • Other control
      • ACTH minimal role
      • Response is blunted by 1-2 days with chronic ACTH elevation
      • Sodium
      • Must be a drop in sodium
      • Atrial natriuretic peptide
      • Decreases renin secretion to decrease AT II levels
        • Decreased responsiveness of adrenal to ATII
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10
Q

Hyperadrenocorticisms

A

Abnormalitites, both clinical and chemical, that results from excessive, chornic exposure to glucocorticoids regardless of etiology

Pituitary - excess ACTH due to pituitary tumor

Adrenal-autonomous cortisol secretion due to adrenocortical carcinoma or adenoma

Hypothalamic - pituiary hyperplasia due to ecess corticotropic-releasing hormone

Iatrogenic - excess glucocorticoid administration

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11
Q

Cushing disease

A

HAC due to an ACTH producing pitutiary tumor

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12
Q

Cushing Syndrome

A

Clinicla signs due to glucocorticoid excess from any cause

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13
Q

Canine Hyperadrenocorticism

Pituitary Dependent Hyperadrenocorticism

A

Most common ~85% of cases

Excess adrenocorticotropic hormone (ACTH) production bu the pars distalis of hte pituitary gland

Microadenoma: <1cm in diameter

Signs due to excessive ACTH and subsequent excessive cortisol production, with a loss of negative feedback

Macroadenoma: up to 15%, >1cm in diameter

Signs due to excessive ACTH and subsequent excessive cortisol production

Bilateral adrenal hyperplasia

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14
Q

Canine Hyperadrenocorticism

Adrenal Dependent Hyperadrenocorticism (ADH)

A

Less common: 15% of all cases

Autonomous production of cortisol

Adenoma ~50% benign

Carcinoma ~50% malignant, local extension, metastasis to liver and lungs

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15
Q

Canine Hyperadrenocorticism

Signalment

Age

A

middle-aged to older

rare for HAC to occur in any dog <6yrs

Dogs with ADH are usually older than dogs with PDH

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16
Q

Canine Hyperadrenocorticsm

signalment

Sex

A

Females slightly overrepresented

Accountif for 55-60% of dogs with PDH

account for 60-65% of dogs with ADH

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17
Q

Canine Hyperadrenocortisms

Signalment

Breed

A

PDH: smaller preed dogs more common

ADH: ~50% >20kg, rest small breed

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18
Q

Canine Hyperadrenocorticism

Clinical Signs

Polydipsia and Polyuria

A

85-97% of dogs with HAC

Glucocorticoids interfere with antidiuretic hormone release and activity, resulting in polyuria

Polydipsia is compensatory

Normal water consumption

Polydipsia >100ml/kg/d

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19
Q

Canine Hyperadreonocorticism

Clinical signs

Polyphagia

A

Occurs in most dogs with HAC

Glucocorticoids have direct stimulatory effect on the appetite

Ravenous appetite

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20
Q

Canine Hyperadreonocorticism

Clinical signs

Pendulous Abdomen

A

>80% of dogs with HAC

Due to: Redistribution of fat to the abdomen

muscle wasting of the abdominal muscles

Hepatomegaly

Often misinterpreted was weight gain by the owner

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21
Q

Canine Hyperadreonocorticism

Clinical signs

Panting

A

Wasting of muscle of respiration

Reduced capability of thoracic expansion from the distended abdomen

muscle weakness

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22
Q

Canine Hyperadreonocorticism

Clinical signs

Infections

A

Urinary tract infections

Pyoderma, respiratory, oral cavity

Unusual organisms causing infection

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23
Q

Canine Hyperadreonocorticism

Clinical signs

Muscle weakness / loss

A

excessive protien catabolism and muscle wasting

24
Q

Canine Hyperadreonocorticism

Clinical signs

Dermatologic Changes

A

Bilateral changes

Symmetrical truncal alopecia and thin skin

Hyperpigmentation and comedones

calcinosis cutis

Bruising

Poor wound healing

Pyoderma

25
Q

Canine Hyperadreonocorticism

Clinical signs

Cardiovascular effects

A

sodium and water retention results in hypertension and hypervolemia

26
Q

Canine Hyperadreonocorticism

Clinical signs

Neurologic signs

A

Anorexia, behavioral changes, and disorientation, circling, central blindness, or other neurologic signs

10-15% of dogs with PDH in association with a macroademona

27
Q

Canine Hyperadreonocorticism

Clinical signs

Repro

A

Negative feedback on pituitary gonadotropin secretions

Decrease in testicular androgen production in males

Anestrus in females

28
Q

Canine Hyperadreonocorticism

Clinical signs

Others

A

Myotonia

facial nerve paralysis

Diabetes mellitus

Proteinuria / hypoalbuminemia

Pulmonary thromboemboli

Hypercoagulable state

29
Q

Canine Hyperadrenocorticism

Diagnosis

A

Can be a diagnostic delimma because no test is highly sensitive or specific

Cortisol cna be elevated due to non-adrenal illness

Clinical signs compatible but diagnostics don’t support clinical suspicion

Other steroid production causing clinical signs

30
Q

Canine Hyperadrenocorticism

Diagnosis

Minimum Data Base

A
  • CBC
    • stess leukogram
    • Thromobocytosis
  • Chemistry
    • Elevated liver enzymes (ALP>ALT)
      • ALP:
        • Primarily due to the GC-induced isoenzyme
        • Secondary to mild intrahepatic cholestasis from glycogen deposistion
      • ALT:
        • variable mild hepatic necrosis, glycogen storage, swollen hepatocytes
      • Hypercholestrolemia
        • due to stimulated lipolysis
      • Hyperglycemia
  • Urinalysis
    • always perform with HAC regardless of urine sediment
  • Blood Pressure
    • hypertensive
  • Radiographs
    • Hepatomegaly, ectopic clacification, Adrenal tumor, Osteoporosis, Cystic Calculi
31
Q

Canine Hyperadrenocorticism

HAC Testing

A

Two step process

  • Screening:
    • Confirms clinical suspicion of HAC
  • Differentiating Test
    • Choose appropriate treatment plan
      • Medical - Pituitary dependent
      • Surgical - adrenal dependent
32
Q

Canine Hyperadrenocorticism

HAC Testing

Screening Test

A

THere is NO Perfect test

A postive test result should never be the sole basis of your diagnosis

Adrenocorticotropic hormone stimulation test

Low Dose Dexamethasone Suppression test

Urine Cortisol:Creatinine ratio

33
Q

Canine Hyperadrenocorticism

HAC Testing

Screening Test

ACTH Stimulation Test

A

Sensitivity - PDH

Specificity - PDH and ADH

Chronic stress or non-adrenal illness may produce test results suggestive of HAC

Advantages:

Fast - 1 hour to preform

good choice if non-adrenal illness is suspected

ONLY WAY TO DIAGNOSE IATROGENIC HAC

Disadvantages - EXPENSIVE

34
Q

Canine Hyperadrenocorticism

HAC Testing

Screening Test

Low Dose Dexamethasone Suppresion Test

A

Procedure: baseline cortisol; injection dexamethasone IV, Collect serum samples 4 hrs and 8 hrs post injection

Interpretation:

Normal - suppressio of plasma cortisol at 4 and 8 hrs

HAC - no suppression at 4 or 8 hrs

PDH - may exhibit suppression form baseline cortisol

May exibit normal suppression at 4 hrs but escape into anbormal range at 8 hrs

35
Q

Canine Hyperadrenocorticism

HAC Testing

Screening Test

Low Dose Dexamethasone Suppresion Test

Advantages

A

Good choice for non-adrenal illness is not suspected

Is a differentiating test if suppression followed by escape

Inexpensive

36
Q

Canine Hyperadrenocorticism

HAC Testing

Screening Test

Low Dose Dexamethasone Suppresion Test

Disadvantage

A

Takes 8 hours to perform

37
Q

Canine Hyperadrenocorticism

HAC Testing

Screening Test

Urine Cortisol: Creatinine Ratio

A

Best used to determine if a dog does NOT have HAC

Sensitivity - nearly 100%

Consistently high serum cortisol results in proportionately high amount excreted in the urine

Negative Results rules out HAC

38
Q

Canine Hyperadrenocorticism

Differentiating Test

Goal

A

differentiate pituitary dependent vs. adrenal dependent hyperadrenocorticsm

Abdominal ultrasound

high dose dexamethasone suppression test

endogenous ACTH meausurement

39
Q

Canine hyperadrenocorticism

Differential tests

Abdominal ultrasound

PDH

A

bilateral adrenal hypertrophy

overlap in normal adrenal gland size and hypertrophy

Threshold of 7.4mm diameter = 77% sensitivity and 80-91% specificity

40
Q

Canine hyperadrenocorticism

Differential tests

Abdominal ultrasound

ADH

A

Unilateral adrenal enlargement, contralateral atrophy

Presence does not equal functional adrenal mass

41
Q

Canine hyperadrenocorticism

Differential tests

HIgh Dose Dexamethasone Suppression Test (HDDST)

A

Procedure - same as LDDST except use 0.1mg/kg

ADH - do not suppress at 4 or 8 hours

PDH - will suppress at 4 or 8 hours

Failure to suppress means the odds of having PDH vs. ADH is 50-50 because ADH never suppress but PDH is the most common form

42
Q

Canine hyperadrenocorticism

Differential tests

Endogenous ACTH levels

A

Not used clinically

Advantages - can positively differentiate PDH vs. ADH

Diasadvantages - difficult to measure

43
Q

Canine hyperadrenocorticism

Differential tests

Computed Tomography (CT)

A

diagnosis of adrenal tumors

pituitary tumors when macroadenoma present

44
Q

Canine hyperadrenocorticism

Differential tests

Magnetic Resonance Imaging (MRI)

A

more accurate for visualization of small pituitary tumors but only 50% of dogs with PDH will have identifiable microadenoma

45
Q

Pituitary Dependnet HAC

Medical Management

A

TREATMENT OF CHOICE
Necrosis of adrenal cortex - fasiculata and reticularis most susceptibel

Enzyme inhibitors in steroid synthesis pathways

trilostane

ketoconazole

L-Deprenyl

46
Q

Pituitary Dependent HAC

Trilostane

A

FDA approved for dogs - therapy of choice in US

Competitive inhibitor of 3B hydroxysteroid dehydrogenase → inhibits production of progesterone and 17-hydroxyprogesterono → inhibits adrenal cortisol and aldosterone

47
Q

Pituitary Dependent HAC

Trilostane

Efficacy

A

sings improve within a few weeks of starting drug. Marked improvement within 2 months.

enzyme inhibition rapidly reversible if dugs is discontinued

48
Q

Pituitary Dependent HAC

Trilostane

Adverse Effects

A

transient vomiting, diarrhea, lethargy

rarely, hypoadrenocorticism may develop

Adrenal necrosis causing death is a rarely reported adverse effect

49
Q

Pituitary Dependent HAC

Trilostane

Monitoring therapy

A

There is no single protocol shown to be superior to another

ACTH stimulation test is recommended on the trilostane insert.

10-14 days after starting trilostane

2 weeks after dose increase

every 3 months for the long term

50
Q

Adrenal Dependent HAC

Surgical Treatment

A

TREATMENT OF CHOICE
unilateral adrenalectomy if metastatic disease and invasion absent of adjacent structures is absent

51
Q

Adrenal Dependent HAC
Surgery

Complications

A

Perioperative complications: hemorrhage, pulmonary thromboembolism

Post-Operative complications: acute adrenal insufficiency, organ fialure/vascular

52
Q

Adrenal Dependent HAC

Surgery

Prognosis

A

MST 36 month if benign and easily removed and the patient survives the first two weeks

Malignant tumors have less favorable prognosis

53
Q

Adrenal Dependent HAC
Medical Options

A

Mitotane: necrosis of adrenal cortex, may also have effects on metastatic lesions, often requires longer induction phase and higher dose for maintenance pase

Trilostane: no efficacy reported

54
Q

HAC prognosis

PDH

A

most treated dogs experience imporved quality of life and show a reduction in clinical signs, reduced morbidity, and alleviation of long-term complications associated with untreated disease

Persistence or development of CNS signs carries a guarded to poor prognosis without intervention to address pituitary enlargement

55
Q

HAV prognosis

ADH

A

benign adrenal tumors carry a good/excellent prognosis after successful removal.

Malignant tumors have a guarded to grave prognosis

Medicine 1 VCS860 (13 decks)

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