Patho/Pharm Exam 2 review

Cardiac Glycosides (digoxin)

Strengthen the heart’s contractility to treat heart failure

SE: arrhythmias, rash, headache, toxicity

Beta Blockers (metoprolol and carvedilol)

Competitively blocks B1 receptors to treat hypertension, heart failure, angina, a-fib

SE: Bradycardia, hypotension, bronchospasm

Atorvastatin

Treats hyperlipidemia by inhibiting HMG-CoA reductase enzyme, which reduces cholesterol synthesis and increases LDL receptors in liver.

SE: GI upset, UTI, insomnia, myalgias

DO NOT USE in patients with liver failure/disease

ACE inhibitors (Lisinopril)

Reduces levels of angiotensin II, which dilates blood vessels, reduces blood volume, and prevents pathologic changes in the heart and blood vessels. Used to treat hypertension, heart failure, and MI.

SE: hypokalemia, dry cough, angioedema

Preload

volume of blood received by heart (stretch)

Afterload

resistance the heart must overcome to eject blood (squeeze)

Atherosclerosis

Plaque build-up that narrows arteries

Left coronary artery

“the widowmaker” - if this artery is occluded…no good

Stable angina

chest pain with exertion; relieved with rest

caused by coronary artery disease

Unstable angina

Chest pain at rest

Caused by coronary artery disease, thrombus, emboli, vasospasm

Variant angina

Chest pain that comes and goes caused by a coronary artery spasm

NSTEMI

when blood flow to coronary artery is PARTIALLY blocked off

STEMI

when blood flow to coronary artery is COMPLETELY blocked off

Troponin

Common lab bc it is released as a byproduct of cardiac cell death

Myocardial infarction

Death of cardiac cells & muscle

B-natiuretic peptide (BNP)

released by the ventricles when overworked; causes vasodilation

Right-sided heart failure

Usually secondary to left-sided HF

Can be also caused by pulmonary issue

Left-sided heart failure

Impaired pumping of blood to the body

Blood backs up from left heart into lungs

S/S: hacking cough, crackles and wheezing in lungs, fatigue, weakness, nocturia (fluid retention), angina

water soluble hormones

Bind to receptors on the cell’s surface (rapid)

lipid-soluble hormones

Enter cell and change gene expression (slower and longer-lasting)

Upregulation of receptor response

Receptors will be more sensitive to hormone over time due to small amounts of hormone being produced

Downregulation of receptor response

Receptors will have less affinity for hormone because there is too much of it

Ex. type II diabetes - insulin receptors have been desensitized to insulin

ADH - INCREASES fluid

Stored and released from pituitary

Secreted due to increased serum osmolality and decreased BP

Acts on kidney by helping with water reabsorption

Diabetes insipidus - “Dry Inside”

Body not secreting enough ADH

Central or nephro

S/S: polyuria (peeing 3-4 gallons/day), increased thirst, hypernatremia, hyperosmolality

Interventions: Replacing ADH, hydration

SIADH - “Soaked Inside”

Too much ADH secretion - holding on to a lot of water

Medication induced or tumors

S/S: hyponatremia, weakness/fatigue, muscle cramps, nausea, postural BP changes, anorexia

Interventions: water restriction

Aldosterone - INCREASES fluid volume

Released in response to decreased BP, decreased sodium, or increased potassium LIKE CORTISOL

Promotes water and sodium retention

Stimulates potassium excretion in kidneys

Natriuretic Peptides - DECREASES fluid volume

Made in heart

Released in response to excessive stretching of heart muscles

Oppose renin-angiotensin-aldosterone system

Increases excretion of sodium and water

Cortisol

Main stress hormone

Released in response to stress, low blood glucose

Counteracts insulin —> hyperglycemia

Reduces bone formation and muscle growth (energy going elsewhere)

Increases sodium and water retention and excretes potassium LIKE ALDOSTERONE

Addison’s disease

adrenocorticol insufficiency

S/S: weakness, hypotension, hypoglycemia, hyperpigmentation, hyperkalemia, weight loss

Interventions: hormone replacement

Cushing’s disease

Hypercortisolism

S/S: moon face, truncal obesity, buffalo hump, hisutism, muscle wasting, thin skin, petechiae, glucose intolerance, hypertension, hypokalemia

Interventions: based on etiology

Cardiac output calculation

HR x stroke volume = CO

Type II Diabetes Mellitus

Insulin receptors are resistant

Long-term effects of unmanaged hyperglycemia: neuropathy, HPTN, retinopathy, slow wound-healing

Type I Diabetes Mellitus

Pancreas is not producing any insulin

Medications: insulin only

Insulin

Moves glucose into cells to lower blood glucose levels

Metformin

MOA: inhibits glucose production in liver and sensitizes insulin receptors

SE: decreased appetite, nausea, diarrhea, lactic acidosis

Nursing considerations: caution if renal issues, limit alc use, hold prior to IV contrast

Glipizide

MOA: Stimulates insulin release from pancreas

SE: hypoglycemia, drug interactions

Nursing considerations: monitor for hypoglycemia, caution in liver/renal issues

GERD

Backflow of gastric contents into esophagus

Caused by: decreased sphincter strength

Meds: PPIs, H2 receptor antagonist, antacids

Gastritis

Inflammation of the stomach and small intestines

Can be acute (infection) or chronic (inflammatory disorder)

Gastroenteritis

Caused only by infections

Peptic ulcer disease (PUD)

Ulcer that causes burning pain, typically on empty stomach

Relieved by eating or antacids

Caused by: H. pylori, NSAIDS, ETOH/smoking

CAUTION —> glucocorticoids can lead to PUD

IBS

S/S: cramps, abdominal pain, diarrhea/constipation

Unknown cause

IBD

Crohn’s disease: Inflammation of terminal ileum causing diarrhea, abd pain, cramping

Ulcerative colitis: inflammation of colon and rectum causing abd pain, rectal bleeding, severe colitis

Liver failure

ACUTE: severe damage to liver (usually caused by acetaminophen toxicity)

CHRONIC: damage to liver over time (often caused by chronic alcohol consumption)

S/S: jaundice, weakness, increased bleeding portal hypertension, ascites (fluid build-up caused by portal hypertension)

Stimulant laxative (senna)

6-12 hr onset

Stimulates peristalsis to move stool

Osmotic laxative (Polyethylene glycol)

1-3 day onset

Draws water into stool to soften

Stool softener (docusate)

1-3 days onset

Creates surfactant to help stool slide

PPI (omeprazole)

MOA: block proton pumps to decrease stomach acid production

SE: increased risk of fractures

Pressure ulcers

Caused by lack of blood flow to an area over a body prominence

Risk factors: immobility, moisture, nutrition, friction, sensory percpetion

Stage 1: skin intact, unblanchable redness

Stage 2: Partial thickness, dermis exposed

Stage 3: Full thickness, subcutaneous fat may show

Stage 4: Full thickness, muscle and bone visible

Unstageable: slough or eschar covering wound underneath

Burns

1st degree: red skin, no blistering, rarely need medical intervention

2nd degree: partial thickness, blistering, 3-4 weeks healing

3rd degree: full thickness, nerve damage, edema, can lead to loss of function due to extensive scar tissue

Treatment: fluid resuscitation - lactated ringers as electrolyte replacement

Skin changes expected with age

decreased elasticity

decreased cell turnover

decreased moisture and nutrient supply

thinning and increased fragility

capillary fragility

Osteoclasts

dissolves and reabsorption of bone

Osteoblasts

building bone

Osteoporosis

Disease in which bone reabsorption is faster than bone formation that causes low bone density

More common in women

Common fracture sites = spine and hip

Risk factors: age, sex, genetics, ETOH, smoking, corticosteroid use, decreased calcium

Rhabdomyolysis

Acute condition caused by extensive muscle injury

Release of proteins and electrolytes affect heart and kidneys

Complications: hyperkalemia, hypocalcemia, acute kidney injury, compartment syndrome

Caused by: drug overdose, physical exertion, direct muscular damage

Inflammation phase

1-6 days after tissue injury

Platelets, neutrophils, macrophages

Proliferation phase

1-2 weeks

growth factors

Clot forming

Epithelialization

Remodeling phase

can be up to 2 years

scar formation (avascular)

tissue regeneration