Final Exam Blueprint; forgetting angina, similarities w cancer

Myasthenia Gravis

Chronic autoimmune breakdown of acetylcholine receptors (AChR) at the neuromuscular junction

Clinical Manifestations of Myasthenia Gravis

Drooping of eyelids (ptosis), diplopia, swallowing weakness, muscle weakness that improve with rest

Treatment for Myasthenia Gravis

Pyridostigmine/neostigmine — increases ACh at NMJ; corticosteroids; thymectomy

Myasthenitic crisis

Life-threatening condition typically with respiratory failure from weakening of diaphragm (triggered by physical or emotional stress)

Atrial Fibrillation (A-fib)

Atria quivers instead of contracting effectively, causing irregular and fast heartbeat; increases risk of clots

Risk factors related to Afib

HTN, CAD, HF, hyperthyroidism, diabetes, obesity, sleep apnea, advanced age

Pathophysiology of Atrial Fibrillation

Stretching/scarring of atria remodels electrical patterns, causing uncontrollable firing and loss of atrial kick

Lab abnormalities related to dehydration

↑ Sodium, ↑ Hct/Hgb, ↑ BUN/creatinine, ↑ urine specific gravity, ↑ serum osmolality

↓ GFR

How does the body regulate dehydration?

RAAS (releases aldosterone) and ADH

Normal BUN

7-20mg/dL

Normal Creatinine

0.7-1.3mg/dL (men); 0.6-1.1 mg/dL (women)

Aldosterone

Directs kidneys to reabsorb more sodium, excrete potassium → Water follows sodium back into ECF to retain fluid

Antidiuretic Hormone (ADH)

Signals kidneys to reabsorb water and concentrate urine when there’s low BP, high blood osmolality, or dehydration

Renin

Enzyme released by kidneys when blood pressure or blood volume is low

Renin-Angiotensin-Aldosterone Mechanism

Renin + Angiontensinogen → Angiotensin I (lungs) → Angiontensin II → Adrenal cortex → Aldosterone

Angiotensin II

Vasoconstricts and stimulates aldosterone release; from angiotensin I

Excess Renin and Aldosterone

Excessive amount produced causes hypertension, fluid retention edema, hypokalemia (muscle cramps)

Low Renin and Aldosterone production

Too little production causes hypotension (dizzy), dehydration, hyperkalemia, risk of shock (hypovolemia)

Erythropoietin

Hormone produced by kidney that increases proliferation and maturation of stem cells into blood cells in bone marrow

Stimuli for EPO

Low oxygen levels (hypoxia), anemia, decreased renal perfusion, high altitudes

Normocytic

RBCs are normal size (MCV)

Normochromic

RBCs have normal color, meaning a normal amount of hemoglobin

Low EPO

Underproduced due to CKD → Normocytic, normochromic anemia → fatigue, dyspnea, pallor, decreased oxygen carrying capacity

Excess EPO

Excess erythropoietin → polycythemia → increased blood viscosity → risk of clots and HTN

Excess ADH (SIADH)

Too much water retained → hyponatremia and low & concentrated urine

Low ADH

Kidneys fail to absorb water → severe dehydration, large volume of dilute urine, hypernatremia

Hypogylcemia symptoms

Sweating, tremors, irritability, tremors, confusion, hunger, pallor, cyanosis, sleepiness

Severe Hyperglycemia

Cells cannot use glucose, starving cells of energy (causes lipolysis) and increasing concentration of blood

Osmotic diuresis

Glucose exceeds renal threshold → glycosuria → water follows glucose → polyuria, dehydration, electrolyte loss

Macrovascular Effects of Chronic Diabetes

Atherosclerosis causing coronary artery disease (vessels in heart), stroke, peripheral arterial disease (vessels in limbs)

Microvascular Effects of Chronic Diabetes

Damage to small vessels from blood sugar being too toxic:

-Retinopathy (vision loss)

-Nephropathy (weakens kidneys → proteinuria → renal failure)

-Neuropathy (nerves)

Atherosclerosis from Diabetes

High blood sugar damages endothelial vessels → more permeable to lipids, inflammation triggered chronically (attracts macrophages and fatty plaques)

Diabetic Ketoacidosis (DKA)

Ketones excessively produced due to lack of glucose uptake in cells in T1DM, causing blood to become acidic

Ketone Production

Body breaks down fat for acid product ketones which provides energy when there’s little glucose from fasting or exercising

DKA symptoms

-Fruity breath (one of ketones in DKA is acetone, which has fruity scent)

-Kussmaul respirations (acidic blood causes metabolic acidosis)

Hyperosmolar Hyperglycemic State (HHS)

Excess glucose in bloodstream → high concentration of solutes in blood → excessive urination to balance → severe dehydration

-No significant ketone build up due to insulin being present (T2DM)

HHS symptoms

Severe dehydration, neurological changes (confusion, seizure, coma) due to high blood glucose in brain

Hyperglycemia general symptoms

-Polydipsia, polyuria, polyphagia

-Loss of volume (hypotension, tachycardia)

-Confusion, lethargy, possible coma (HHS or DKA)

-Electrolyte imbalances (insulin needed to bring K into cell)

Infections from Chronic Diabetes

Diabetes can cause poor immune function, high glucose supporting bacterial growth, and deficient wound healing → possible amputation

Diabetic Foot Ulcers from Chronic Diabetes

Foot ulcers created due to:

-Neuropathy (can’t feel pain, pressure, injuries, so wounds go unnoticed)

-Ischemia (impaired wound healing from lack of oxygen and nutrients)

Thyroid hormones

Hormones primarily involved in metabolism and protein synthesis while also affecting growth and development

Thyroid synthesis

TSH from pituitary → thyroid follicular cells produce T4 (inactive, 4 iodine) that convert to T3 in cell (active form); iodine is essential

Thyroid transport

T4 typically binds to thyroid-binding globulin in blood (70% of transport proteins)

Thyroid regulation

Hypothalamus (TRH) → pituitary (TSH) → thyroid (t3/t4)

Negative feedback of thyroids

-High T3/T4 → ↓ TRH and TSH

-Low T3/T4 → ↑ TRH and TSH

Hyperthyroidism

↑ T3/T4, ↓ TSH

High metabolism and increased sympathetic system:

-Weight loss, heat intolerance, sweating, tachycardia, tremors, increased BMR, goiter, insomnia

Hypothyroidism

↓ T3/T4, ↑ TSH

-Fatigue, weakness, difficulty gaining/losing weight, cold intolerance

-Dry, rough pale skin, coarse dry hair, hair loss

-Muscle cramps and aches

-Constipation, depression, memory loss

Grave’s Disease

Autoimmune thyroid stimulating antibodies activating TSH receptors → excess thyroid hormones

Grave’s Disease symptoms

Enlarged thyroid (goiter), bulging eyes, hyperthyroid symptoms

Causes of Cerebrovascular accidents (stroke)

-Ischemic (87%) — obstruction of blood flow to brain (thrombotic, embolic); causes MI

-Hemorrhagic (13%) — rupture of BVs due to HTN, aneurysm, or arteriovenous defect; higher fatality

Stroke Risk Factors

HTN (highest), Afib, diabetes, smoking, hyperlipidemia, obesity

Transient Ischemic Attack (TIA)

Temporary cerebral flow stoppage that resolves before MI occurs; no damage; warning sign for stroke

Ischemic Stroke

Caused by clot blocking blood flow; one-sided weakness, facial droop, speech problems

Hemorrhagic Stroke

Most fatal type of stroke; spontaneous rupture of cerebral blood vessel; sudden thunderclap headache, vomiting, neuro deterioration

Thrombotic Stroke

Most common type of stroke due to atherosclerosis; causes aphasia, neglect, vision loss

Lacunar Stroke

Micro infarcts of deep brain vessels due to HTN, smoking, diabetes; causes pure motor or sensory deficits

Embolic Stroke

Fragment of thrombus breaks off and travels in bloodstream (lungs, brain); linked to Afib, MI

What should be done before giving anticoagulant for stroke?

Verify the stroke isn’t hemorrhagic (CT scan), otherwise anticoagulant increases bleeding

Treatment for Stroke

Rule out hemorrhage first, tPa to dissolve clots and restore blood flow, aspirin for ischemic stroke (if no tPa present), BP control

Ischemic Penumbra

Area around damaged core of brain that contains weakened cells that are salvageable if perfusion returns quickly

Metabolic Alkalosis

Loss of metabolic acids with increases in bicarbonate concentrations, causing hypoventilation to keep CO2

What causes metabolic alkalosis?

Hypokalemia, excess bicarbonate (antacids), low acids (vomiting, gastric suction)

Respiratory alkalosis

Anxiety/panic, pain, fever, sepsis, pregnancy, high altitudes (breathe faster for O2)

Metabolic acidosis

Poisoning (methanol, ethylene, glycol), loss of HCO3, increased acid (DKA, lactic acidosis, renal failure)

Respiratory acidosis

COPD, asthma, airway obstruction, opioids, neuromuscular weakness

What does a high anion gap indicate?

Loss of HCO3 from DKA, lactic acidosis, toxins, extra acids

Respiratory compensation for metabolic acidosis

Hyperventilation → expels and lowers PaCO2 (Kussmaul respirations)

Respiratory compensation for metabolic alkalosis

Hypoventilation → retains PaCO2

Normal CO2

35-45 mmHg

Normal HCO3

22-28 mEq/L

Normal pH

7.35-7.45

Normal Blood Glucose

70-100 mg/dL

Hypoglycemia

Low blood sugar from excess insulin, missed meals, or overexertion; rapid onset, requires immediate glucose intake

Gastroesophageal Reflux Disease (GERD)

Impairment of lower esophageal sphincter leading to reflux of gastric acid into the esophagus, damaging/scarring esophagus and irritation

Patient Education for GERD

-Elevate HOB

-Eat small meals and avoid lying down 2-3 hours after

-Avoid late meals and trigger foods (caffeine, alcohol, citrus, fatty/spicy foods)

-Smoking cessation and avoid tight clothing

-PPI meds, H2 antagonists

Peptic Ulcer Disease (PUD)

Open sores or ulcers in lining of stomach, duodenum, esophagus due to imbalance between acid production and mucosal lining, causing erosion of tissue

Causes of PUD

H. pylori and long-term NSAIDs weaken stomach’s protective mucus and lining, causing acid to have a more corrosive effect and forming ulcers

Treatment for PUD

PPIs to reduce acid, antibiotics for H. pylori, and avoid NSAIDs, smoking, & alcohol

Melena

Black, tarry stool from digested blood; indicates upper GI (stomach, duodenum, esophagus)

Hematochezia

Bright red blood; indicates lower GI bleed (colon, rectum) OR severe/massive upper bleed

Paralytic Ileus

Loss of intestinal movements causing lack of food movement → abdominal distention, no bowel sounds, no gas, no stool

Paralytic Ileus Interventions

-Keep patient NPO to rest bowel

-NG tube to decompress stomach

-IV fluids to prevent dehydration and replace electrolytes (esp. potassium)

-Early ambulation to stimulate motility

Ulcerative Colitis

Chronic autoimmune inflammation bowel disease (IBD) starting from rectum to colon

Complications of UC

Bloody diarrhea, urgency, abdominal pain, anemia, fatigue, risk of colon cancer

Irritable Bowel Syndrome (IBS)

Functional GI(all) disorder with abdominal pain, bloating, and altered bowel habits (diarrhea, constipation or both);

NO bleeding, inflammation or damage

Liver Cirrhosis

Chronic liver scarring → liver replaces damaged cells with scar tissue → impaired liver function

Causes of Liver Cirrhosis

Hepatitis, alcohol abuse, fatty liver disease, other conditions that cause prolonged liver inflammation

Liver cirrhosis physical symptoms

Jaundice, ascites, edema, bruising, portal hypertension, hepatic encephalopathy, RUQ discomfort

Labs indicating Liver Cirrhosis

Increased bilirubin, ammonia, PT/INR

Decreased albumin, platelets

Liver

-Produces bile for digestion

-Metabolizes drugs, toxins

-Stores glycogen and vitamins

-Makes albumin and platelets

-Converts ammonia to urea

Bleeding Esophageal Varices

Dilated veins in walls of lower part of esophagus causing bleeding due to chronic liver disease with portal hypertension

Tumors

Masses formed from overgrowth of cells

Cancer origin

Cancer from original site (breast cancer → lung cancer (still breast cancer))

Benign Neoplasms

Slow tumor growth expansively (outwards), but does not invade or spread (localized); well-differentiated

Malignant Neoplasms (metastatic)

Tumors grow rapidly and spread widely, has potential to kill regardless of position, compresses blood vessels and outgrows their own blood supply

Staging of Cancer

TNM (tumor, node, metastasis)

In situ (stage 0)

Stage where abnormal cells haven’t spread elsewhere

Localized (stage 1)

Small tumor contained in one place

Regional (stage 2)

Tumor cell grows larger and now near lymph vessels/nodes

Regional (stage 3)

Tumor cell grown deeper into tissues and spread to nearby lymph nodes