Patho Exam 1

Where is aldosterone produced?

The adrenal glands.

What triggers aldosterone’s release?

Angiotensinigen II (which also stimulates peripheral arterial vasoconstriction, raising BP)

What organs are directly involved in RAAS?

Kidneys, liver, lungs, adrenals.

Addison’s disease

Adrenals fail to produce enough aldosterone and cortisol; rare endocrine disorder.

Where is ADH produced?

The hypothalamus.

Where is ADH stored before being released into the bloodstream?

The posterior pituitary.

Which organ is responsible for metabolizing aldosterone?

The liver

What does hyperaldosteronism lead to?

Fluid retention (hypervolemia, edema, ascites), hypokalemia (can’t stop excreting potassium), alkalosis (can’t stop excreting hydrogen).

SIADH

Too much ADH = retain too much water

What’s the opposite of SIADH?

Diabetes Insipidus

Diabetes Insipidus

Kidneys are unable to prevent the excretion of water. Body does not produce or respond adequately to ADH.

Where is albumin produced?

In the liver

What indicates hyperkalemia on an ECG?

Wider QRS and peaked T-wave

What indicates hypokalemia on an ECG?

Depressed ST, low W wave, prominent U-wave

Anaplasia

When cancerous cells lose maturation and specialization, and are able to produce substances they normally don’t.

What is paraneoplastic syndrome and how often does it occur?

When cancerous cells produce substances (such as hormones) mimicking other areas of the body and causing secondary problems; occurs in 20% of cancer patients.

What is glomerulonephritis?

Inflammation of the glomeruli. Two types.

Nephritic Syndrome

Inflammation and immune system activation in the glomeruli; causing hypertension, oliguria, and hemanaturia (blood in the urine).

Nephrotic Syndrome

Glomeruli are damaged by any number of sources (diabetes, lupus, amyloidosis, etc.), causing massive proteinuria.

Uremia

Lit “blood in the urine”; kidneys fail to filter waste from blood.

What are the four mechanisms of fluid regulation?

ADH, RAAS, thirst, sympathetic nervous system (vasoconstriction/vasodilation)

When aldosterone goes up, what electrolytes are excreted?

K+ and H+

Cushing’s and Conn’s disease

Too much adrenal hormones, including aldosterone.

What is the most important factor of colloid osmotic pressure?

Plasma proteins, especially albumin.

If the liver is damaged, what are two impacts on fluid pressure?

Albumin production and aldosterone production both occur here.

What are some signs and symptoms of fluid volume deficit?

Pulse, BP, tissue turgor, weight loss, ins vs. outs, capillary refill, mucous membranes and tearing.

What are some signs and symptoms of fluid volume overload?

Breath sounds, quality of breath, mental status, neck veins.

What are some clinical manifestations of hypovolemia?

Increased hematocrit, BUN, creatinine, electrolytes, albumin, urine concentration, temperature (sans infection).

What are some clinical manifestations of hypervolemia?

Weight gain, hypertension, edema, decreased hematocrit and other blood levels.

What are some signs/symptoms of hyperkalemia?

Numbness/tingling of the extremities, muscle cramping, diarrhea, apathy, mental confusion, at risk for cardiac arrest.

What are some signs/symptoms of hypokalemia?

Nausea, vomiting, sluggish bowel, cardiac arrhythmias, postural hypotension, muscle fatigue, weakness.

Why might you give insulin and glucose to someone experiencing hyperkalemia?

Insulin moves K+ into cells (out of ECF). Give glucose alongside it just to keep insulin balanced.

Azotemia

Retention of wastes in the blood (urea, creatinine) etc.

Characteristics of benign tumors

Well-defined, slow-growing, non-invasive, well-differentiated cells, do not metastasize, low mitotic index.

Characteristics of malignant tumors

Fast-growing, ill-defined borders (not encapsulated), invasive, infiltrative, high mitotic index, poorly differentiated cells, do metastisize.

Hyperplasia

Number of cells increase, tissue enlarges

Dysplasia

Abnormal cell growth within a tissue

Proto-oncogenes

Normal non-mutant genes that code for cellular growth

Oncogenes

Mutant genes that direct protein synthesis and cellular growth TOO FAST (as though a brick is on the accelerator)

Tumor-Suppressor Genes

Encode proteins that negatively regulate proliferation

What are famous examples of proto-oncogenes?

Her2-neu, Ras, MYC

What are famous examples of tumor-suppressor genes?

BRACA1, BRACA2, p53, Rb

How does chronic inflammation predispose a person to cancer?

Stimulates a wound-healing response that includes proliferation and new blood vessel growth.

What is cancer’s mass effect?

Ex. cancer in the brain displaces the brain and compresses it against skull/compresses nerves and arteries, results in secondary effects.

Paraneoplastic syndrome

Cancer cells in the body begin releasing hormones, neurotransmitters, proteins, or substances that the body interprets as those things, and then responds as if they were released from the correct gland or organ. So additional syndromes or disorders develop in addition to the cancer as the body reads these substances as "real" chemical messages.

Cachexia

Most severe form of malnutrition; body essentially starts eating itself.

What is Stage 1 cancer?

Confined to its organ of origin.

What is Stage 2 of cancer?

Cancer is locally invasive.

What is Stage 3 of cancer?

Cancer has advanced to regional structures.

What is Stage 4 of cancer?

Cancer has spread to distant sites.

Clinical manifestations of hyponatremia

Cellular swelling with cerebral edema leading to headache, stupor, and coma; muscle weakness; decreased thirst; edema if secondary to hypovolemia.

Clinical manifestations of hypernatremia

Cellular shrinking with CNS irritability; increased thirst; dry mucous membranes; hypotension with oliguria (low urine output) if secondary to hypovolemia.

PTH and calcium relationship

PTH increases blood calcium. 

Calcitonin and calcium

Calcitonin acts on the kidneys and bones to remove calcium from ECF

Vitamin D and calcium

Vitamin D sustains normal plasma levels of calcium and phosphate by increasing their absorption from the intestine.

Clinical manifestations of hypocalcemia

Increased neuromuscular activity; muscle cramps; tremors; skeletal muscle tetany; hyperactive reflexes.

Clinical manifestations of hypercalcemia

Decreased neuromuscular activity (stupor to coma); renal calculi; bone pain; decreased reflexes.

Chvostek’s Sign

Involuntary twitching of facial muscles from light tapping due to hypocalcemia. 

Pyelonephritis

Acute infection/inflammation of the upper UTI, specifically renal pelvis/kidney insterstitium.

Stage 1 CKD

Screen for risks, eGFR is normal (greater than or equal to 90) but other signs suggest possible kidney damage.

Stage 2 CKD

Eliminate or reduce risk factors - meds manage causes of kidney disease; eGFR 60-89.

Stage 3 CKD

Slow progression of disease; change diet and meds manage renal disease directly; eGFR 30-59.

Stage 4 CKD

Manage complications, prepare for dialysis; eGFR 15-29.

Stage 5 CKD

Dialysis, transplant; eGFR less than 15.

CKD impacts on cardiovascular

High risk for electrolyte imbalances (esp K+), heart failure (hypertension, hypervolemia, anemia).

CKD impacts on pulmonary

Dyspnea/tachypnea; crackles; pulmonary effusions; pulmonary edemas

Neuro impacts from CKD

Uremia can lead to: lethargy, peripheral neuropathy, asterixis, decreased alertness/cloudy mental state; poor fine motor skills/balance; if untreated delirium, seizures, coma, death.

CKD impact on skin

Uremia can lead to yellow or darkening of skin, pruritis, uremic frost.

CKD impacts on skeleton

Elevated phosphorus (= not enough calcium); inability to activate Vitamin D; PTH pulls calcium from bones, leading to bone remodeling/brittle bones = renal osteodystrophy.

How does anemia from CKD lead to heart failure?

Not enough red blood cells makes the heart have to work harder to get enough oxygen to our tissues. 

What heart failure impacts lead directly to CKD?

Reduced cardiac output, chronic hypoperfusion, increased venous pressure.

Metaplasia

One mature cell type is replaced by another mature cell type.

Dysplasia

Abnormal changes in the size, shape, and organization of cells in a tissue or organ.

Clinical manifestations of pylenephritis

Flank/groin pain, fever, chills, costovertebral tenderness or pyuria.

When is a patient at risk for pylenephritis?

UTI, urinary cath, pregnancy, neurogenic bladder, vesicouretal reflux.

eGFR

Estimates how well your kidneys are filtering; a kidney filtering speedometer; should be greater than 90 mL/min.

Why are three different diseases all called diabetes?

Diabetes means “passing through” and all have to do with urine output. Mellitis means “sweet” (extra glucose in the urine) and Insipidus means “tasteless” because it has nothing to do with sugar.

How does Aldosterone impact eletrolytes?

Adosterone increases sodium reabsorption and increases potassium secretion.