Path 1 - Endocrine 3

pbhati17's version from 2017-03-01 14:07

Endocrinology 6.3: Adrenal Gland

Review of Adrenal Phsyio

Question Answer
Adrenal Gland: Shape? Location?Bean-shaped, Medial to the kidneys
Adrenal Gland cross section reveals?Yellow Cortex, Reddish-brown medulla
In normal dogs, the Adrenal cortex is?Firm, Yellow, Uniform thickness
In normal dogs what is the Adrenal Gland cortical/ medulla ratio?2:1
Up to 75-90% of the Adrenal Gland produces over _ different steroid hormones?50
Histologically the Adrenal Cortex consists of 3 zones, the _, _ & _Zona Glomerulosa (Salt)
Zona Fasciculata (Stress)
Zona Reticularis (Sex)
Zona Glomerulosa is what % of the cortical mass? Where is it located?15% (Salt controlling hormones), Outermost zone
The Zona Glomerulosa produces? Specifically?Mineralocorticoids, Aldosterone (Salt)
What is the fxn of Aldosterone?Na+ & K+ Homeostasis via kidney & sweat glands
Aldosterone czs retention & loss which electrolytes? What effect does this have?Na Retention, K Loss, Expansion of ECF; ↑ Blood Pressure
What system controls Aldosterone release?Renin-Angiotensin Aldosterone System (RAAS) & to a lesser extent: ACTH
The Zona Glomerulosa is necessary for regeneration of?The other 2 zones
Zona Fasciculata is what % of the cortical mass? Located?70%(Sugar controlling hormones), Middle zone
The Zona Fasciculata produces? Specifically (2)?Glucocorticoids, Cortisol & Corticosterone (Stress)
What balance do Cortisol & Corticosterone have the greatest effect on? Which metabolisms are acted upon?Glucose Homeostasis; Carbohydrate metab, Protein metab, Lipid metab
What effect do Cortisol & Corticosterone have on Carbohydrate Metab? What does this result in?↓ use of CHO's & 'sparing' of Glucose via Gluconeogenesis (make new glucose from non-CHO substrates) resulting in Hyperglycemia
What effect do Cortisol & Corticosterone have on Protein Metab?Protein Catabolic (USE ALLLLLL THE PROTIENS!!)
What effect do Cortisol & Corticosterone have on Lipid Metab? What does this lead to?Lipolysis, Release of glycerol & Free Fatty Acids
Gluconeogenesis (GNG) is the generation of glucose from? Ex?Non-CHO carbon substrates
- Lactate
- Glycerol (FAT)
- Glucogenic Amino Acids (PROTEINS)
GNG occurs mainly in the _ & is enhanced in states of _(3), etc.Liver; Fasting, Starvation, Intense Exercise
Cortisol & Corticosterone cz/inhibit?Hyperglycemia
Increase Glucose Production
Inhibit the action of insulin
Suppression of inflammation & healing (this is why you use hydrocortizone on allergic inflammation like bug-bites)
Cortisol & Corticosterone cz wound dehiscence though the inhibition of (3)?Fibroblast proliferation
Collagen synthesis
Immune response
Zona Reticularis is what % of the cortical mass? Location?15% (Androgen hormones), Innermost zone
Zona Reticularis produces? Specifically?Sex hormones (Androgens in both males & females)
Effects of excess androgen secretion depend on(3)?Which steroid is secreted
Sex of the individual
Age of onset
Embryogenesis of the Adrenal cortex arises from?Mesoderm
Embryogenesis of the Adrenal medulla arises from?Neuroectoderm


Question Answer
Hyperadrenocorticoidism (Cushing’s) → CS? (Effect on skin? Blood cells? BP? Musculoskeletal system? Metabolism? & some others)Ascites
SKIN: Alopecia, Cutaneous Calcinosis, Thin skin
Musculoskeletal: Weakness, MM wasting
BLOOD: Eosinopenia, Lymphopenia, Mature neutrophilia (Stress leuko)
BP: Hypertension
Apparent obesity (changes where body fat gets stored in the body - from the arms & legs to around the face, back of the neck & the stomach)
↑ concentration of urinary ketosteroids
Metabolic derangements e.g., Diabetes (insulin inhibiting hormone)
Hypoadrenocorticoidism (Addison’s) → CS?ELECTROLYTE IMBALANCES:
Cardiac Failure
What are 3 czs of adrenocortical hemorrhage?Trauma in newborn
Severe stress
Septicemia/toxemia (Waterhouse-Friderichsen Syndrome)
What are the 4 general czs of Adrenitis?VIRUSES
What does Adrenitis look like (gross & micro) if the cz is viral? What is an example?Multifocal necrosis, w/ intranuclear inclusion bodies. Eg: herpesvirus
What TYPE of bacteria cz Adrenitis? (Examples?) Of these types, what are the 2 kinds of ADRENITIS which result?Usually Gram NEGATIVES such as actinobacillus & salmonella. This results in a necrosuppurative adrenitis. HOWEVER, it can ALSO be czd by mycobacteria. This results in a granulomatous adrenitis
What type of fungi can cz Adrenitis? What are some examples? What is the type of adrenitis they cz?Czd by DIMORPHIC fungi, such as Histoplasma capsulatum, Coccidioides immitis or Cryptococcus neoformans. Fungal infection leads to granulomatous adrenitis
Which parasite is capable of czing Adrenitis & what does it look like?Toxoplasma gondii, which produces necrosis w/ an infiltration of histiocytes in the adrenal cortex of many species of animals (mind control your stress)
Fxnal proliferative lesions in ferrets → How common is this? What are some influencing factors on the prevalence of it?2nd most common neoplasm in adult ferrets!! The female ferrets are over double as likely to develop this as males & animals gonadectomized at an early age are also more prone (bc of chronic trophic stimulation of the zona reticularis by LH)
What are the 2 different types of lesions in Fxnal Proliferative Lesions in Ferrets? How common is each difference?(1) Bilateral enlargement (45% of cases), diffuse or nodular hyperplasia
(2) Unilateral enlargement (55% of cases), adrenal cortical adenoma or carcinoma
What are the CS/Fxnal disturbances for Fxnal proliferative lesions in ferrets?Vulvular enlargement
Endometrial hyperplasia
Squamous metaplasia of prostatic ductular epithelium & cystic prostatic dz
↑ plasma concentrations of estradiol-17β (a CONSISTENT FINDING)
Bilaterally symmetrical alopecia (esp. ventral abdomen & medial aspects of rear legs)
Polyuria/Polydipsia (PU/PD)
Palpable mass at the cranial pole of the kidneys (left > right)
*What is a CONSISTENT finding in the case of fxnal proliferative lesions in ferrets?↑ plasma concentrations of estradiol-17β (ferrets are moody bc of all the estrogen)
Hypercortisolism (Cushing’s) → Who is this most common in?Most common in dogs, less so in horses & rare in all other animals
What are the 3 Major Pathogenic mechanisms of hyperadreno? How common are they? (Actually need to know this) (Just name & %, more details in other cards)1⁰ hyperadrenocorticism (10-15%)
2⁰ hyperadrenocorticism (80%)
Pharmacological (iatrogenic) hyperadrenocorticism (5-10%)
**What is happening in 1⁰ hyperadrenocortisism?Usually czd by a Cortical Neoplasm, especially Adenoma OR an Idiopathic Adrenocortical Hyperplasia
**What is happening in 2⁰ hyperadrenocorticism?Bilateral Cortical Hyperplasia due to ↑ ACTH from pituitary tumor (Pituitary Dependent Hyperadrenocorticism (PDH))
What is happening in Pharmacological (iatrogenic) hyperadrenocorticism?Over administration of glucocorticoids by the doctor


Question Answer
**Explain what Ectopic ACTH syndrome is?This is a PARANEOPLASIA!
Various cancers, such as:
Small Cell Lung Cancer
Carcinoid tumor
Pancreatic Islet Cell Tumors
Medullary Carcinomas of the Thyroid
- Can spontaneously produce ACTH which can result in HypERcortisolism
***CS of HypERcortisolism are dependent on the general effects of cortisol itself. Effects on proteins, sugars & fats & Role in inflammation?Cortisol is Glyconeogenic
Protein Catabolic → MUSCLE WASTING (so, makes sugar but breaks down proteins & fats)
Anti-inflammatory effects (Corticosteroids)
How does excess cortisol affect the renal system?Polyuria/polydipsia (due to hyperglycemia? (Osmotic diuresis) Effect on ADH? (Too much cortisol, save Na so lose K, hypokalemic tubules less responsive to ADH → more pee) )
How does hypercortisolism affect appetite?(Think, it's a steroid & steroids make you hungry) Cz polyphagia... he says "due to direct &/or tumor effect on Hypothalamus" (hunger center of brain)
**How does hypercortisolism affect the liver?HEPATOMEGALY! Due to steroid hepatopathy, ie. ↑ glycogen in hepatocytes bc stimulates gluconeogenesis
How does hypercortisolism affect the abdomen (outside appearance) & why is this?Pendulous abdomen (due to mm atrophy & weakness (protein catabolic) & hepatomegaly)
**How does hypercortisolism affect the skin?It czs dermal atrophy (catabolic processes, affects elasticity of skin & makes it thinner)
Bilateral Symmetric Alopecia (atrophy of hair follicles & sebaceous glands)
Dystrophic Mineralization of the skin ("Calcinosis Cutis"), lung, mm & stomach (due to altered collagen & elastin)
What is the effects of excess cortisol on inflammation & infxn (Immune system)?Cortisol is ANTIINFLAMMATORY, w/ immunosuppressive affects → Eosinopenia & Lymphopenia/Lymphoid involution! Bc of this anti-inflammatory & immunosuppressive combo, the animal has ↑ susceptibility to infxns
What are the 2 types of HYPOadrenocortisism?1⁰ & 2⁰
What is going on in 1⁰ HYPOadrenocortisism?In MOST CASES, the problem is Bilateral Idiopathic Adrenal Cortical Atrophy. Other czs may be bilateral destruction of adrenal glands (such as in adrenitis/infarction/non-fxnl tumor, etc), or IATROGENIC (sudden withdrawal following prolonged excessive administration of synthetic steroids-- adrenal isnt used to making as much ACTH as now needed)
*Which cz of 1⁰ HYPOadrenocortisism is most common?Bilateral Idiopathic Adrenal Cortical Atrophy
**Bilateral Idiopathic Adrenal Cortical Atrophy → Who is this most common in? Why does this happen? What are the main results of this on the adrenal gland & what is most concerning? (Not clinical signs yet)MOST COMMON type of 1⁰ Addison’s & its most common in young to middle-age female dogs. This is an autoimmune/inherited disorder which can result in destruction of ALL 3 CORTICAL LAYERS → deficient production of all cortical hormones. Why does this matter? Bc deficiency of mineralocorticoids can be lethal
Bilateral destruction of adrenal glands → What are some czs for this?Inflammation
Explain how iatrogenic 1⁰ hypoadrenocortisism worksIf there is a sudden withdrawal following prolonged excessive administration of synthetic steroids, the pituitary hasn't had to make much ACTH up to that point bc there were ↑ levels of steroid already (neg feedback) & the adrenal cortex hasn't had to be synthesizing it, but suddenly you take away the steroid & the pituitary needs time to catch up & make more & the adrenal cortex needs time to make more
***Lymphocytic Infiltration in Adrenal Cortex w/ destruction of cortical tissue czing Adrenalitis can lead to?Idiopathic Atrophy & Addison's Dz
*Which type of hypoadrenocortisism affects MINERALCORTICOID PRODUCTION?1⁰!! (Not 2⁰)


Question Answer
What czs 2⁰ hypoadrenocortisism? What are the main results of this on the adrenal gland?ACTH deficiency from destructive pituitary lesion-> this results in trophic atrophy of only the ACTH-dependent zones (fasciculata & reticularis), which means mineralocorticoids are not affected → thus, no electrolyte imbalances, which is the most important part of Addison’s
**What is the hallmark clinical sign of Addison’s?HYPERKALEMA! (cortisol is sodium saving & potassium losing. so no cortisol means sodium losing & potassium saving)
**What is the general energy level of an animal with Addison’s?Lethargic w/ stress intolerance
How does Addison’s affect the heart/blood?Bradycardia (electrolyte imbalance)
Changes in the ECG (K+ balance is off)
Acute circulatory failure, i.e., cardiogenic / hypovolemic shock (vasodilation)
**How does Addison’s affect the GI?Anorexia
Vomiting/Diarrhea (non-specific gastroenteritis) → dehydration & emaciation
***What are 3 main electrolytes affected by Addison’s & how are they affected?K - HYPERKALEMIA (hypokaluria) → Weakness & Bradycardia
Na - HYPONATREMIA (hypernaturia)
Cl - HYPOCHLORIDEMIA (hyperchloriduria)
How does Addison’s affect blood sugar levels?Hypoglycemia (from failure of gluconeogenesis & ↑ sensitivity to insulin)
Why are there cardiovascular disturbances in ADDISONS?Bc unlike in Cushing’s, there is a HYPERKALEMIA!! Which severely affects the heart
**How does Addison’s affect the skin?In chronic cases, you will see hyperpigmentation due to an excess of pituitary MSH that develops reciprocally to a ↓ of an inhibitory cortisol (reduced negative feed-back)
Explain how Addison’s affects the adrenal gland itselfThe cortex will be reduced to 1/10 or less of its normal thickness & consists primarily of the adrenal capsule. The medulla on the other hand is relatively more prominent making up the bulk of the gland
What is a Pheochromocytoma?Most common neoplasms in the adrenal medulla of animals
Who does a Pheochromocytoma happen in most often? (What might it be concurrent with?)Occurs mainly in dogs & cattle (often concurrent thyroid C cell tumors in bulls & humans → multiple endocrine neoplasia syndrome)
Extraadrenal pheochromocytomas (paragangliomas) → How common & where does this occur?Occur infrequently in the abdomen
Gross appearance of a pheochromocytoma & how can it behave?Often large (greater than 10 cm in diameter), Lt-brown to yellow-red & can be unilateral or bilateral & encapsulated. There is a risk of a pheochromocytoma invading the vena cava & metastasizing extensively (vena cava runs near the adrenal gland). Arteriolar sclerosis & widespread medial hyperplasia of arterioles have been reported in dogs (clinically: paroxysmal hypertension)
Are pheochromocytomas usually fxnl or nonfxnl? (Explain what happens either way)(Remember this is a neoplasm of the adrenal MEDULLA) Darely fxnl ; if so, can czs tachycardia, edema & cardiac hypertrophy
How do you Dx if the tumor in the adrenal gland is a pheochromocytoma?“Chromaffin reaction” where application of K-dichromate or iodate (e.g., Zenker’s solution) to a freshly cut surface will result in a dark-brown coloration in 5-20 minutes if POSITIVE

Recent badges