Cortex:

a) Mineralcorticoids (aldosterone)

b) glucocorticoids (cortisol)

c) androgens (DHEA)

Medulla:

a) catecholamines (epi, NE)

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CRH (hypothalamus) secreted with stress, fever, surgery, trauma, hypoglycemia, SNS -->

ACTH (ant pituitary) secreted in relation to circadian rhythm (highest levels just before waking) -->

cortisol (adrenal cortex)

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Aldosterone

1) secreted by

2) acts where? doing what?

3) impact of serum K

1) secreted by adrenal cortex (*doesn´t belong to hypoth/pituitary heirarchy)

2) acts on the renal tubule. Na+ reabsorbed (H2O follows, incr BP), K+ excreted.

3) hyperkalemia = aldosterone secretion.

hypokalemia suppresses ald secretion.

Iatrogenic Cushing's (hypercortisolism):

MOST COMMON CAUSE OF CUSHING'S

Cushing's Syndrome

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Cushing’s Disease: pituitary adenomas

Cushing’s Syndrome:

What does chronic exogenous glucosteroid administration do to the HPA?

FYI: HPA = hypothalamic-pituitary-adrenal axis: CRH-->ACTH-->cortisol

Iatrogenic Cushing's Syndrome (excess exogenous cortisol)

Adrenal Insufficiency b/c there is no stimulus to restart cortisol release.

Solution:

1) Taper down doses while monitoring HPA axis as well as cortisol alert bracelets.

2) Use short tx of steroids with alternate days.

Diagnostic Triad for Primary

Hyperaldosteronism (conn's disease).

What is the cause?

1) HTN (180/110)

2) hypernatremia

3) hypokalemia

Adrenal Adenoma is cause.

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Cause: high aldosterone

Effect: low renin

Cause: high renin

Effect: high aldosterone

What disorder? Name some causes.

Secondary Hyperaldosteronism

Caused by: renal artery stenosis & edema states (CHF, cirrhosis, nephrotic syndrome)

Conn's Disease

Catopril is ACEi.

Measure baseline plasma aldosterone (PA), give catopril, measure PA after 90 min.

Nml: Suppression of RAAS = decr PA

Abml: incr PA = aldosterone secretion independent of RAAS.

Conn's Disease Diagnosis.

1) PRA level

2) PA level

3) electrolytes

4) pH balance?

5) BP

6) Specific Drug test

1) PRA level: decr plasma renin activity

2) PA level: incr plasma ald

3) electrolytes & pH: hypokalemia (w/ assoc metabolic alkalosis), hypernatremia

5) BP= HTN

6) Specific Drug test: Captopril

Western World: 70% cases are autoimmune

Worldwide: infectious diseases more common (TB, fungal, CMV)

2º adrena insuff due to pituitary failure from sudden cessation of corticosteroids is ACUTE ADRENAL INSUFF and life threatening

Lab results:

-Low cortisol, high ACTH

-Low Ald, low K, high Na

acute adrenal insuff

Lab results:

low ACTH, low cortisol

nml electrolytes

Mngt/Tx of Addison's Disease

HRT-

-replace glucosteroids w/ hydrocortisone (**can cause cushings syndrome**).

-replace mineralcorticoids with fludrocortisone (monitor with PRA/PA).

Glucocorticoid replacement doses:

1) during acute illness, surgery, trauma

2) intercurrent illness

3) severe illness

4) post-HRT

1) during acute illness, surgery, trauma - stress doses

2) intercurrent illness - double maintainence dose

3) severe illness- possibly 4-5x maintainence dose at times

4) post-HRT - possible requierment of stress doses up to 1 yr.

Pheochromocytoma (catecholamine secreting tumor of the adrenal medulla).

Rare, 80% unilat.

FYI: Paroxysmal hypertension is episodic HTN

Lab results:

Incr plasma normetanephrine & metanephrine.

pheochromocytoma dx (almost)

Must get CT/MRI to check for tumor and administer clonidine test.

Dx of Pheochromocytoma:

-clonidine, a centrally-acting alpha-2 agonist used to treat HTN. Clonidine mimics catecholamines in the brain, causing it to reduce the activity of the sympathetic nerves controlling the adrenal medulla. A healthy adrenal medulla will respond to the clonidine suppression test by reducing catecholamine production; the lack of a response is evidence of pheochromocytoma.

Where are the following found and what do they do?:

1) follicles

2) parafollicular cells

THYROID GLAND: composed of....

1) follicles: selectively absorb iodine (as iodide ions) from blood.

-Colloid, a rich protein called thyroglobulin, inside of the follicles synthesizes (iodine + thyrosine w/ TPO enzyme) and stored thyroid hormones.

2) parafollicular cells (aka C Cells) secrete calcitonin*

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*Calcitonin: reduces serum calcium, opposing PTH effects. 

T3 & T4 bound to TBG = inactive.

Unbound = active.

TRH (Hypothalamus) -->

TSH (Anterior Pituitary) -->

T3/T4 (Thyroid Gland)

Hypothyroidism:

What is the most common form in the US?  Worldwide? 

US: Hashimoto's thyroiditis (primary hypothyroidism) aka chronic lymphocytic thyroiditis

Worldwide: iodine def

antibodies against thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland.

What is this condition and what are 2 risk factors?

Hashimoto's Thyroiditis (primary hyperthyroidism)

Risks: white, female

• Lethargy/fatigue
• Hoarse Voice
• Impaired memory/decr cognitive function
• Cold Intolerance
• Weight Gain
• CHF symptoms
• dry skin/eyes
• anorexia, nausea, constipation
• decr libido/fertility, menorrhagia

Pt presents tired and sleepy with slurred speech b/c of macroglossia (enlarged tongue).  Eyes are dry.

Skin/Hair/Nails: course, dry, cold skin; lateral eyebrow thinning, peri-orbital non-pitting edema

CV: BP is 125/110, bradycardic, distant cardiac sounds

Abdomen: distended, decr bowel sounds

Musculoskeletal: decr strength, delayed DTR, carpal tunnel syndrome.

What is your dx?  What do you want to palpate and how would it feel?

Hypothyroidism

Thyroid gland may be non-palpaple or diffusely enlarged w/ rubbery/asym nodules (at first), then small.

Hypothyroidism:

FYI-

Macroglossia is the medical term for unusual enlargement (hypertrophy) of the tongue.

Keratoconjunctivitis sicca (KCS), also called keratitis sicca, sicca syndrome, xerophthalmia, dry eye syndrome (DES), or simply dry eyes

Pt presents with impaired mentation, hypothermia, hyponatremia, hypoglycemia.

Infection, cold exposure, trauma, CNS depressents, and old age can be causes of this condition. 

Menopausal females b/c they are at higher risk for CV events. 

Incr TSH, T3/T4 nml.

Lab results:

-high titers of antiTPO, antiTSH, antiTg

-decr: total T4, free T4

-elevated TSH

-incr chol, TG

-Pernicious Amenia

-Decr total T4

-decr free T4 (FT4)

-Incr TSH

1) neonates - congenital hypothroidism can lead to cretinism if untreated - dwarfism w/ mental retardation)

2) postmenopausal women - to lower CV/osteoporosis risks. (15% of subclinical cases)

3) elderly - to rule out hypothyroidism as a cause of dementia and depression.

Levothyroxine replacement therapy.  Monitor TSH 6-8wks after beginning/changing therapy. 

Preggers: incr dose b/c prenatal vitamines/iron decr TH absorption.

Elderly: lower dose

Contraindications: slow, small doses, esp with CV risks....angina/MI/CHF pts not started on TH until CV problems are stabilized (think of the function of TH on CV: similar to catecholamines...)

Most common cause of hyperthyroidism.

Graves disease- is an autoimmune disorder, in which the body produces antibodies to the receptor for thyroid-stimulating hormone (TSH).  These antibodies cause hyperthyroidism because they bind to the TSH receptor and chronically stimulate it, resulting in

abnormally high production of T3 and T4. This in turn causes the clinical symptoms of hyperthyroidism, and the enlargement of the thyroid gland visible as goitre.

-irritability, anxiety, restlessness, difficultly concentrating, insomnia

-fine tremor

-Eye: injection, lacrimation, diplopia

-wt loss, loss stools, incr appetite

-CV: SOB, palps, possible angina/HF/afib w/ underlying condition

-heat intol, diaphoresis

-oligomenorrhea (never get pd)

-tetany of hands (low Ca b/c malabsorption)

Precpitating factors (infection, trauma, surgery) can cause high fever, delerium, N/V, dehydration, afib, hypotension.

Lab: catecholamine levels nml.

Dx and tx?

Thyroid storm - life threatening, severe thyrotoxicity.

Tx- IV iodide to decr TH release, steroids to inhibit T4 to T3 conversion.

incr T3, FT3, T4

decr TSH

Tx:

-propythiouracil (PTU), methimazole (antiTH drugs)

-b-blocker (sx relief)

-radioactive iodine therapy (choice for adults)

What is this tx for?  When would you do surgery?

Thyrotoxicosis.

Surgery - subtotal thyroidectomy:

-no response to meds

-pregnancy (radioactive iodine ablation C/I)

-large goiters

Pt presents with neck pain radiating to jaw/ear, fever, myalgia, lymphocytosis, incr ESR, T3/T4 initially high then low, low RIAU.  Acute illness.

-What condition?

-Duration?

-Tx (3 drugs)? (what is NOT effective?)

Subacute thyroiditis

subsides in 2-8 wks

NSAIDS

Initial stage - b blocker (if severe)

second stage - TH replacement

Not effective - antiTH meds

pt presents with mailaise, fatigue, weight loss, nml/slightly elevated ESR, painless.

What condition?

Tx? (what is not effective?)

postpartum thyroiditis

Usually no need to treat b/c its mild.

Second stage - TH replacement.

Not effective - antiTH meds

Thyroid nodules:

-what % is cancer?

-common

-rare (3)

-sx

Thyroid nodules:

-what % is cancer? 10-20%

-common nodule: colloid nodules

-rare (3) nodules: adenoma, cyst, CA.

-sx: usu asx.  Dysphagia, sx/signs of hyper/hypothyroidism.

You find a fixed, rapidly growing thyroid nodule w/o mov't upon swallowing in a male elderly pt. 

What do you suspect?

How would you make the dx?

Thyroid cancer

Dx with fine needle aspiration (biopsy)

The physical exam of a 29 yo asymptomatic, euthyroid man shows 2 fixed nodules.  The best diagnostic test is:

Hyperglycemia, ketosis, acidosis...caused by the breakdown of fatty acids into ketones  (liver converts to glucose/ketone bodies) when there is too little insulin/too much counter regulatory hormones.

Dx? (in what pt population?)

Causes?

Diabetic Ketoacidosis (acute complication of mostly Type I DM)

Causes: acute stress or decr insulin

Sx: polyuria, polydipsia, lethargy, weakness, nausea, anorexia. 

PE: decr turgor, tachycardia, orthostatic HTN, sweet odor

Lab: low electrolytes, incr serum glucose

Sever hyperosmolarity and severe hyperglycemia are the hallmarks.

What dx and in what pt population?  Mortality?

Hyperosmolar Hyperglycemic State (HHS) - acute complication of mostly type II diabetics.

Mortality up to 50%.

1) rehydrate

2) gradually correct hyperglycemia

3) K supplement

Hypoglycemia

bg<60...you get sx.

bg<50...obtunded mentation.

Prolonged state= IRREVERSIBLE BRAIN DAMAGE.

Hypoglycemia

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1) microvascular (retinopathy & nephropathy)

2) Neuropathic

3) Macrovascular (atherosclerosis)

DM nephropathy is the leading cause of ESRD in the US.

Affects what % of what type of diabetics?

1st sign?

30-35% type I diabetics

Microalbuminuria is 1st sign.

This DM neuropathy is distal and symmetric.  Pain and tingling in stocking-glove formation.

What is it and what do you see in its late stages?

Diffuse DM neuropathy.

Late stages: severe sensory loss, smooth muscle wasting, neuropathic arthropathy, focal ulceration.

DM autonomic neuropathy has a poor prognosis.  List the sx assoc with the following organ systems

-Cardiac

-Vascular

-GI

-GU

-Cardiac: incr HR (decr HR responsiveness), incr silent ischemia risk/CHF/sudden death.

-Vascular: orthost HTN

-GI: constipation, hypo/hypermotility, pancreatic insuff

-GU: overflow incont, ED, bladder hypomotility

Metabolic syndrome is also known as syndrome X, insulin resistance syndrome.

Into abdominal fat via catheter

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Sulfonylurea (GLYBURIDE)

Meglitanide (REPAGLANIDE)

Biguanide (METFORMIN)

Thiazolidinediones - TZDs (¨GLITAZONES¨)

a synthetic version of Amlyn, which is produced by pancreatic beta cells in response to meals. given sc; for type I, or type II who use insulin; may cause hypoglycemia

Adults (2005-2006 stats)

34% obese

33% overweight

Soluble: attracts water, forms gell, trapping carbs to slow glucose absorption - BG regulator; increase transit time, decr nutrient absorption because active enzyme activity, high binding capacity for ions and lipids

Insoluble: decr transit time, facilitiate regularity (incr fecal bulk), lignin is the only binder.

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Acute phase of protein during stress, infection, inflammation. 

What is it?

Increased when...

High levels signify...

C-Reactive Protein (CRP)

Incr CRP when alb/prealb decr

Incr CRP sign of nutritional risk during stress/trauma

Lab Assessment:

1) Protein metab

2) carb metab

3) lipid metab

1) Protein metab: creat/BUN

2) carb metab: glucose, prot bound glucose (1 wk), HbA1c (2-3 mos)

3) lipid metab: Tot Chol, HDL, LDL, TG

SKIN Clinical Sx of Nutritional Disorder

1) obesity/DM

2) vit K/C def

3) marasmus, niacin, biotin, riboflavin, zinc, essential FAs

4) zinc

5) DM, kwashiokor

1) obesity/DM acanthosis nigricans

[image]

2) vit K/C defcy ecchymosis

3) marasmus, niacin, biotin, riboflavin, zinc, essential FAs defcy dermatitis

4) zinc defcy psoriasisform rash

[image]

5) DM, kwashiokor pressure ulcers

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ulcerating dermatosis on a Malawian child suffering from kwashiorkor

Clinical Sx of Nutritional Disorders:

1) hair sx of zinc, biotin def

2) nail sx of iron def

3) lack of iodine

4) mouth: lack of riboflavin

5) mouth: lack of fluoride

6) neuro: niacin, thiamin, vit E def

7) Neuro: thiamin

8) neuro: vit D, Ca

1) hair sx of zinc, biotin def - alopecia

2) nail sx of iron def- spoon nails (koilonychia)

[image]

3) lack of iodine - goiter

4) mouth: lack of riboflavin +... angular stomatitis (Fe), cheilosis(niacin, pyridoxine), bleeding gums(vit C, K)

5) mouth: lack of fluoride - caries

6) neuro: niacin, thiamin, vit E def - dementia/delirium

7) Neuro: thiamin - wrist/foot drop

8) neuro: vit D, Ca - tetany

Hunger/Satiety Regulation:

1) incr w/ fasting, decr with feeding, short-term hunger signal

2) gut hormone made in small intestine lining in response to food intake (esp fat).  Short term satiation signal

3) released from distal sm intestine post-prandial.  short term satiation signal.  Reduced in DM II.

Hunger/Satiety Regulation:

1) incr w/ fasting, decr with feeding, short-term hunger signal.  Ghrelin.

2) gut hormone made in small intestine lining in response to food intake (esp fat).  Short term satiation signal.  Cholecystokinin (CKK).

3) released from distal sm intestine post-prandial.  short term satiation signal.  Reduced in DM II.  Glucagon Peptide-1 (GLP-1).

What quandrant are the following abdominal parts found:

1)liver

2)kidney

3)esophagus

4) spleen

5) stomach

6) pancreas

7) duodenum

8) sigmoid

9) cecum

10) jejunum

1) liver RUQ

2) kidney ALL QUANDRANTS

3) esophagus LUQ

4) spleen LUQ

5) stomach LUQ

6) pancreas Upper Quandrants

7) duodenum LUQ

8) sigmoid LLQ

9) cecum RLQ

10) jejunum Lowe Quandrants

Referred pain to where?

1) AAA

2) gallbladder

3) ureter

4) pancreatitis

5) perforated ulcer

1) AAA to lower back

2) gallbladder to shoulder

3) ureter to groin

4) pancreatitis to back

5) perforated ulcer to RLQ

bruising of the flanks and periumbical cords signify what?

[image]

acute hemorrhagic pancreatitis

-flank: Grey Turner's sign

-periumb: Cullen's Sign: Cullen's sign may appear 1 to 2 days after the onset of anorexia and the severe, poorly localized abdominal pains that are characteristic of acute hemorrhagic pancreatitis. It is also present in massive upper GI hemorrhage and ruptured ectopic pregnancy.

An umbilical node as a sign of malignancy in the pelvic of abdomen

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Sister Mary-Joseph Sign

Insicions on the abdomen suggest what previous surgeries:

1) subcostal (kocher)

2) pfannenstiel

3) Mcburney

4) what is this scar called?

[image]

1) subcostal (kocher) - biliary/hepatic

[image]

2) pfannenstiel - bladder/uterus/fallop tubes/ovarian

[image]

3) Mcburney - appendectomy

[image]

4) Chevron

1) RLQ tenderness with LLQ palp

2) pain w/ right hip extension

3) pain with right hip flex and internal rotation

ACUTE APPENDICITIS abdominal exam findings:

1) Rosvig's sign - RLQ tenderness with LLQ palp

2) Psoas sign - pain w/ right hip extension

3) Obturator sign - pain with right hip flex and internal rotation

biliary disease lingo:

1) gallbladder stones

2) common bile duct stone

3) gallbladder inflammation

4) biliary tract infection

1) gallbladder stones cholelithiasis

2) common bile duct stone choledocholithiasis

3) gallbladder inflammation cholecystitis

4) biliary tract infection cholangitis