Looks like no one added any tags here yet for you.
What is DI (Diabetes Insipidus)?
Disorder caused by antidiuretic hormone insufficiency, results in excess fluid retention.
Patho of DI
Decreased ADH secretion/insensitive ADH receptor in kidney → Nephron does not reabsorb water → Body loses high amounts of water in the urine → Dehydration and hypernatremia.
Etiologies of DI
Neurogenic: Head surgery, brain tumors
Nephrogenic: Renal tubular defect, genetics, drugs
Clinical Manifestations of DI
Polyuria
Polydipsia (thirsty)
Poor skin turgor
Dry mucous membranes
Hypotension
FVD (fluid volume deficit)
Hypernatremia
Hyperosmolality
Complications of DI
Cerebral Hemorrhage
Coma
Seizures
What is SIADH?
Excessive secretion of antidiuretic hormone from the pituitary gland; results in excessive water retention.
Patho of SIADH
Excessive ADH secretion → Fluid retention by kidneys = edema → Dilutional hyponatremia
Etiologies of SIADH
Head Trauma
Tumors
Infection
Stroke
Emphysema (ectopic source of ADH)
Meningitis
Clinical Manifestations of SIADH
Weight Gain
JVD
Crackles
Decreased urine output
Edema
Hyponatremia
Hypoosmolality
Hypertension
Complications of SIADH
Heart Failure
Cerebral Edema
Coma
Seizures
What is Hyperthyroidism?
Increase in secretions of thyroid hormone. High levels of T3 and T4, low levels of TSH.
Patho of Hyperthyroidism
Body produces TSI or gland enlarges → Elevated T3 and T4 → Negative feedback inhibition of pituitary TSH → Low TSH, more hormone secreted → High basal metabolic rate.
Etiologies of Hyperthyroidism
Graves Disease: Autoimmune disorder/ Type 2 hypersensitivity
Toxic Adenoma (gland gets irritated, hyper-secretes hormones)
Toxic multinodular goiter
Clinical Manifestations of Hyperthyroidism
Nervousness
Weight Loss
Hyperactive reflexes
Diaphoresis
Muscle Cramps
Irritability
Tetany
Positive Trousseau sign
Positive Chvostek’s sign
Complications of Hyperthyroidism
Heart Failure
Heart Murmurs
What is Hypothyroidism?
Decrease in secretion of thyroid hormone. High levels of TSH and low levels of T3 and T4.
Patho of Hypothyroidism
Loss of function → Decreased production on thyroid hormone (TH) → Increased production of TSH → Slows basal metabolic rate.
Etiologies of Hypothyroidism
Congenital Thyroid Defects
Autoimmune: Hashimoto Disease
Surgical removal of the thyroid gland (most common cause)
Thyroiditis
Clinical Manifestations of Hypothyroidism
Fatigue
Weight Gain
Constipation
Delayed reflexes
Feeling cold
Sluggishness
What is Hypoparathyroidism?
Decrease in secretion of parathyroid hormone (PTH).
Patho of Hypoparathyroidism
Destruction of gland → Insufficient PTH secretion → Decrease in Ca2 levels → Low Ca2 levels.
Etiologies of Hypoparathyroidism
Damage or removal of parathyroid gland, typically when removing the thyroid gland.
Clinical Manifestations of Hypoparathyroidism
Muscle Cramps
Irritability
Tetany
Positive Trousseau Sign
Positive Chvostek’s Sign
What is Hyperparathyroidism?
Increase in secretion of parathyroid hormone (PTH).
Patho of Hyperparathyroidism
Excess secretion of PTH → Increased bone reabsorption and GI absorption of Ca2 → Feedback system fails so calcium continues to increase → High Ca2 levels
Etiologies of Hyperparathyroidism
Primary: Adenoma, gland hyperplasia (glands are irritated, hyper-secretion)
Secondary: Chronic hypocalcemia
Clinical Manifestations of Hyperparathyroidism
Deep bone pain
Pathological fractures (complication as well)
Renal Damage
Hypercalcemia
Hypophosphatemia
Kidney stones
Cardiac Dysrhythmias
What is Type 1 Diabetes Mellitus (DM 1)?
Results from destruction of pancreatic beta cells which leads to NO production of insulin.
Patho of Type 1 Diabetes Mellitus
Genetic/Environmental Pathway: Activation of Macrophages, T cytotoxic cells, and autoantibodies toward beta cells → Destruction of beta cells with decreased insulin secretion.
Etiologies of Type 1 Diabetes Mellitus
Genetic
Environmental
Immunological
Clinical Manifestations of Type 1 Diabetes Mellitus
Polydipsia
Polyuria
Polyphagia (excessive eating)
Weight Loss
Fatigue
Hyperglycemia
What is Type 2 Diabetes Mellitus?
Results from a decrease in beta cell number or insulin resistance.
What is Insulin Resistance?
Suboptimal response of insulin sensitive tissue (liver, muscle, adipose tissue) to insulin.
What is one of the biggest causes of Insulin Resistance?
Obesity
Patho of Type 2 Diabetes Mellitus
Genetic: Decreased activity of amylin → Decreased beta cell mass and function → Hypoinsulinemia → Increased glucagon → High Blood Sugar
Obesity: Decreased activity of ghrelin → Insulin Resistance → Increased demand for insulin synthesis leads to hyperinsulinemia → High Blood Sugar
Etiologies of Type 2 Diabetes Mellitus
Exact Unknown
Risk Factors: Obesity and Genetics
Clinical Manifestations of Type 2 Diabetes Mellitus
Polyuria
Polydipsia
Polyphagia (excessive eating)
Fatigue
Pruritus (skin irritation, itching)
Recurrent infections (in skin and mouth, yeast infections)
Acute Complications of Diabetes
Hypoglycemia
Diabetic Ketoacidosis (DKA)
Hyperosmolar Hyperglycemia Nonketotic Syndrome (HHNKS)
Hypoglycemia
Abnormally low blood glucose
More common in Type 1 DM
Too much or incorrectly timed insulin or exercise or not enough food
Diabetic Ketoacidosis (DKA)
High blood glucose with serum ketones (metabolic acidosis)
More common in Type 1 DM
Acute complication that develops quickly
Precipitated by illness, stress, noncompliance with insulin administration
Hyperosmolar Hyperglycemia Nonketotic Syndrome (HHNKS)
High blood glucose without serum ketones
More common in Type 2 DM
Develops slower (because the person has insulin)
Precipitated by infection, MI, stroke, acute illness which stresses the already weak functioning beta cells
Chronic Complications of Diabetes
Microvascular Disease: Diseased Capillaries
Macrovascular Disease: Diseased Arteries
Infection
Microvascular Disease: Diseased Capillaries (angiopathy)
Diabetic Retinopathy: Blindness
Diabetic Nephropathy: Kidney Failure
Diabetic Neuropathies: Nerve damage/loss of sensation in the lower extremities and feet mostly
Macrovascular Disease: Diseased Arteries
Cardiovascular Disease: CAD, angina, MI
Ischemic Stroke
Peripheral Vascular Disease: Ulcerations, gangrene, amputation
Infection (DM)
Impaired immunity, hypoxia, decrease perfusion, decreased sensation, delayed wound healing
What is Cushing’s Disease?
Hypersecretion of glucocorticoids (cortisol).
Patho of Cushing’s Disease
Loss of feedback control of ACTH secretion → Constant secretion of ACTH → Increase secretion of cortisol
Etiologies of Cushing’s Disease
ACTH Dependent: Pituitary adenoma; Ectopic secreting non-pituitary tumor (small cell in the lung)
Administration of exogenous steroids (syndrome)
Clinical Manifestations of Cushing’s Disease
Obese trunk
Moon face (edema around the face)
Buffalo hump (fat deposit near shoulder)
Hirsutism (facial hair in women)
Ecchymotic areas (bruising)
Purple straie
Hyperglycemia
What is Addison’s Disease?
Adrenocortical Hypofunction
Patho of Addison’s Disease
Autoimmune destruction of adrenal cortical cells → Adrenal atrophy → Decrease cortisol causes increased ACTH or inadequate corticosteroid and mineralocorticoid synthesis
Etiologies of Addison’s Disease
Autoimmune destruction of adrenal cortical cells.
Clinical Manifestations of Addison’s Disease
Bronze pigmentation
GI distrubances
Weakness
Postural
Hypotension
Complications of Addison’s Disease
Hyponatremia
Hyperkalemia
What is Pheochromocytoma?
Tumor of adrenal medulla resulting in excessive secretion of catecholamines.
Patho of Pheochromocytoma
Excess stimulation of alpha and beta adrenergic receptors → Increased secretion of epinephrine and norepinephrine → Increased peripheral vascular resistance.
Etiologies of Pheochromocytoma
Catecholamine secreting tumor of the adrenal medulla
Clinical Manifestations of Pheochromocytoma
Hypertension
Headache
Tachycardia
Palpitations
Diaphoresis
What is Osteoporosis?
A metabolic bone disease resulting in a reduction in density or mass of bone. Losing more bone than you’re making.
Patho of Osteoporosis
Decreased estrogen → Increase in RANKL (makes osteoclasts which eats bones) → Bone resorption greater than bone deposition → Alterations in bone microarchitecture → Loss of bone mineralization → Diminished bone mass and porous bone.
Etiologies of Osteoporosis
Primary: Postmenopausal
Secondary: Other Conditions
Clinical Manifestations of Osteoporsis
Decreased height
Compression spinal fracture
Kyphosis (spinal curvature)
Decreased bone mass measurements
Pathologic Fractures
Complications of Osetoporosis
Pathological Fractures
What is Osteomyelitis?
Infection of the bone.
Patho of Osteomyelitis
Entry of pathogen (most common Stapphylococcus aureus) and inflammatory response → Pus accumulation in bone → Bone cells become ischemic → Sequestra forms (dead bone tissue) → Involucrum (new bone formation) → Allows sinus tracts to develop and spread disease.
Etiologies of Osteomyelitis
Post-trauma
Vascular insufficiency
MVA (motor vehicle accidents)
Orthopedic hardware
Puncture wound of foot
Clinical Manifestions of Osteomyelitis
Bone pain
Malaise
Headache
Fever
Edema
Erythema over bone
Brodie Abscess (painless abscesses surrounding the wound)
Complications of Osteomyelitis
Sepsis
What is Rheumatoid Arthritis?
A chronic, progressive, systemic, autoimmune disease with inflammation of joints and deformity.
Patho of Rheumatoid Arthritis
T Lymph Activation: RANKL increases → Form pannus (what causes the destruction) → Destruction of cartilage and bone.
B Lymph Activation: Rheumatoid factor is formed and binds with IgG → Inflammatory response → Enzymes destroy collagen → Forms pannus → Destruction of cartilage and bone.
Etiologies of Rheumatoid Arthritis
Unclear
Higher in women
Autoimmune
Clinical Manifestations of Rheumatoid Arthritis
Symmetrical pain in small joints
Swelling
Warmth
Erythema
Anorexia/fatigue
Ulnar drift
Swan neck deformity
Boutonniere deformity
What is Osteoarthritis?
A progressive destruction of cartilage in both synovial and vertebrae joints.
Patho of Osteoarthritis
Loss of articular cartilage → Inflammatory response → New bone formation of joint margins (bone spurs) → Subchondral bone changes → Synovitis and thickening joint capsule.
Etiologies of Osteoarthritis
Risk Factors Secondary: Age, obesity, injury, repetitive trauma
Primary: Idiopathic
Clinical Manifestations of Osteoarthritis
Asymmetric join pain increases with activity
Relieved by rest
Herberden’s nodes (DIP)
Bouchard’s nodes (PIP)
What is Gout?
A metabolic disease marked by increased serum uric acid levels and joint inflammation. Acute
Patho of Gout
Body unable to metabolize purine → Leads to increased uric acid in blood → Uric acid crystals form → Deposit into joints → Inflammatory response.
Etiologies of Gout
Familial
DietC
Clinical Manifestations of Gout
Sudden onset of asymmetric joint pain, usually the big toe
Edema
Warmth
Erythema
Elevated uric acid
Fever
Complications of Gout
Kidney Stones
What is Renal Calculi (Nephrolithiasis, Kidney Stones)?
Stones along the urinary tract.
Patho of Renal Calculi
Supersaturation of one or more salts → Precipitation of the salts form a liquid to solid state → Temperature and pH changes → Growth of stone through crystallization or aggregation.
Etiologies of Renal Calculi
Gender (males are more common)
Age
Geographic Location (hotter areas)
Dehydration
Diet (high calcium, purine, uric acid)
Occupation
Clinical Manifestations of Renal Calculi
Pain in flank and abdomen
Nausea
Vomiting
Cool, clammy skin
Hematuria (frank blood, bright red)
Most common stones
Calcium
Struvite
Uric Acid
What is Acute Cystitis?
Inflammation of the bladder.
Patho of Acute Cystitis
Exposure to pathogen → Pathogen travels upwards → Causing Inflammation
Etiologies of Acute Cystitis
Escherichia Coli (most common cause of a UTI)
VUR (Vesicoureteral reflux, urine back-flow from bladder into ureters and possibly the kidneys)
Indwelling catheters
Obstruction
Clinical Manifestations of Acute Cystitis
Frequency
Dysuria (very painful)
Urgency
Lower abdominal and or suprapubic pain
Low back pain
Elderly may experience confusion and lower abdominal pain
What is Pyleonephritis?
Infection of the ureter, renal pelvis, and interstitial tissue.
Patho of Pyleonephritis
Exposure to pathogen → Pathogen ascends from lower urinary tract or bloodstream → Inflammatory process develops → WBC infiltration → Inflammation renal parenchyma.
Etiologies of Pyelonephritis
Bladder Infection
Indwelling Catheter
Renal Stones
VUR (vesicoureteral reflux)
Clinical Manifestations of Pyleonphritis
Fever
Flank pain
Chills
Dysuria
WBC’s in urine
CVA tenderness (patients typically jump)
Urgency
Frequency
What is Glomerulonphritis?
An autoimmune inflammatory process in the glomerulus.
Patho of Glomerulonephritis
Glomerulus injured from antigen-antibody complexes → Precipitates inflammatory process → inflammatory mediators damage basement membrane of glomerulus → Degenerative changes affect all renal tissue.
Etiologies of Glomerulonephritis
Immunologic (untreated strep throat, most common)
Drugs/toxins
Vascular disorders
Systemic disease
Viral causes
Clinical Manifestations of Glomerulonephritis
Headaches
Maliase
Weight gain
Hypertension
Facial edema
Proteinuria (protein in the urine)
Hematuria
Oliguria
Dysuria
Complications of Glomerulonephritis
Chronic Kidney Disease
What is Nephrotic Syndrome?
Excretion of 3.5g or more protein in the urine per day.