Pathoma Review Flashcards
Cushing Disease at it’s most basic is
Excess Cortisol
What are the Clinical FIndings of Cushings disease and how do they relate to the physiology of Cortisol
- Muscle Weakness: Cortisol breaks down proteins to be used in gluconeogenesis. Remember, it is catabolic and its main goal is to keep glucose in the blood to keep you alive. It will do anything to make sure this happens.
- Moon Fascies, Buffalo Hump, Truncal Obesity: This is due to the relocation of fat. As blood glucose increases, so does insulin. Insulin increases fat storage
- Abdominal Striae: Cortisol inhibits Collagen synthesis, you get thin skin
- Hypertension: Cortisol has a direct effect on vasoconstriction by upregulating Alpha 2 receptors
- Osteoporosis
- Inmmune suppression: Three methods 1) Inhibit phospholipase A2 which means you get no arachidonic acid metabolites which make prostaglandin 2) Inhibit IL-2 3) Inhibit Histamine Release
MMAHOI
Causes of Cushings
1) corticosteroids: These basically are cortisol. ACTH will be low, therefore both adrenals will hypertrophy
2) Adrenal adenoma, carcinoma or hyperplasia: ACTH will be low. Uninvolved gland will atrophy
3) Pituitary adenoma: ACTH will be high. HIGH DOSE DEXAMETHASONE WILL SUPPRESS IT.
4) Paraneoplastic ACTH secretion
HIGH DOSE DEX WON”T TOUCH IT
Hyperaldosteronism presentation
Hypernatremia (actually it is usually normal because the ADH increases water reabsorption so sodium concentration doesn’t get too far out of whack)
Hypokalemia
Metabolic acidosis_ loss of H
Will also see hypertension due to plasma volume increase
Primary hyperaldosteronism will have LOW RENIN
Usually caused by adrenal adenoma
Secondary hyperaldosteronism will show HIGH RENIN
This is most likely due to volume loss or CHF
Congenital adrenal hyperplasia
EXCESS SEX steroids
Most common cause of congenital adrenal hyperplasia is:
deficiency in 21-hydroxylase. This is the enzyme needed to convert Pregnenolone to Mineralocorticoid and Glucocorticoid. WHen its gone, everything is shunted into sex steroids
Why do you get congenital adrenal hyperplasia?
Because without cortisol being made, ACTH secretion skyrockets and we know that whenever ACTH touches the Adrenals, they grow.
Clinical features of congenital adrenal hyperplasia?
- Lack of ADH = no salt, high k, hypotension
- Life threatening hypotension due to lack of cortisol
- Precocious puberty in males, clitoral enlargement in females.
Acute lack of adrenal hormones
Waterhouse Friedrichsen syndrome
What happens in WFS?
Necrosis of the adrenal glands due to DIC.
What causes WFS?
N. Meningitidis usually
What is the cause of death in WFS
Hypotension—-NO CORTISOL
What is Addison’s disease
Chronic insufficiency of the Adrenal glands
Most common cause of Addison’s in the US
Autoimmune
Most common cause of addison’s in the developing wor;d
TB
What color are tumors of the Adrenal Medulla
Brown…..you will see a yellow capsule surrounding a tumor in the adrenal medulla and that is the cortex. Yellow because of Cortisol
mulitnodulat goiter is generally caused by
Iodine deficiency
Are multinodular goiters usually toxic? Toxic meaning they secrete Thyroid hormone without TSH stimulation
No. Usually Euthyroid (non-toxic). Rarely they become TSH independent leading to hyperthyroidism. These are called toxic goiters
What is the cause of the pre-tibial myxedema and exopthalmos in Graves Disease?
Fibroblasts behind the orbit and overlying the shin express TSH receptors. When stimulated they produce glycosaminoglycans which leads to inflammation and edema. The edema is non-pitting, very dough like because there isn’t much water in it/
What is Cretinism?
Hypothyroidism in neonates and infants
Cretinism is cahracterized by
mental retardation, short stature, enlarged tongue, umbilical hernia
Hyporthyroidism in adults
Myxedema
Hyporthyroidism in kids
Cretinism
What are the clinical features of Myxedema due to
Decrease in Basal Metabolic Rate and decreases SNS activity
Clinical signs and symptoms of myxedema
1) myxedema- glycosaminoglycan buildup resulting in deep voice and large
2) Weight gain
3) slowing of mental activity
4) muscle weakness
5) cold intolerance
6) bradycardia
7) hypercholesterolemia
8) constipation
Hyperthyroidism at the beginning of hashimotos
follicle damage
Type 1 diabetes is an autoimmune disease associated with what?
T cell mediated destruction of beta cells
Which HLA types of Type 1 associated with
HLA-DR3 and HLA-DR4
Clinical presentation of type 1
Weight loss, low muscle mass, eat a ton
Explain the polyuria, polydipsia, and glycosuria seen in diabetic patients?
The excess sugar in the system is filtered out by the kidneys to some extent and pulls out water via osmotic diuresis. You pee a lot and becuase of this dehydration you are always thirsty.
Diabetic Ketoacidosis arises when
times of stress like an infection
Why does stress trigger DKA
Epinephrine stimulates glucagon release (remember it counters insulin release) so blood sugar goes way up. Glucagon also increases lipolysis which leads to high FFAs.
The liver converts FFAs to ketone bodies.
All of this results in hyperglycemia over 300, anion gap alkalosis, and Potassium all over the damn place because there is no insulin to dirve it into cells.
How does DKA present?
Weird respirations, dehydration, fruity breath, nausea, vomitting, mental status change
Treat DKA
fluids, insulin, potasssium
Why is secondary diabetes mellitus often present with GH excess?
GH induces gluconeogenesis. It is diabetogenic along with Cortisol.
Diabetogenic Hormones
Epinephrine, Cortisol, GH, GLucoagon
Autoimmune adrenalitis
gradual destruction of the adrenal cortex…causes addison’s disease,,,,chronic adrenal insufficiency..ok
What organs do not need insulin to uptake Glucose
BRICK L: Brain, RBC, Intestine, Cornea, Kidney, Liver
WEAKNESS, VOMITTING, DIARRHEA, hyponatremia, hyperkalemia,
NAME THE Condition: Hypoadrenalism
Hyperosmolar, nonketotic coma
T2D…basically hyperglycemia leads to polyuria which we know, this can cause massive dehydration and glucose can get to ridiculously high levels.
