Patho Flashcards
Hormones travel In the BLOODSTREAM throughout the body.
Endocrine cells secrete hormone into the blood stream
Know
____ ___ associated disorders
Decrease in NUMBER of receptors
Impaired receptor functions
Presence of ANTIBODIES
Surface receptor
___ disorders
Acquired disorders in the post receptor signaling cascades.
Inadequate synthesis of a second messenger
Target cell response problem
Intracellular disorders
Diseases of the ANTERIOR PITUITARY
HYPOPITUITARISM- absence of SOME pituitary hormones or the complete failure of ALL pituitary hormone functions
Causes:
Pituitary INFARCTION Sheehan's syndrome is a condition that affects women who lose a life-threatening amount of blood in childbirth or who have severe low blood pressure during or after childbirth, which can deprive the body of oxygen. Hemorrhage Shock Head trauma (TBI) Infections and tumors
Know
Diseases of the anterior pituitary
PAN HYPOPITUITARISM
ALL pituitary hormones are low, and the individual suffers from multiple complications ACTH deficiency TSH deficiency FSH & LH deficiency GH deficiency ADH deficiency
Know
___ is commonly caused by A slow growing pituitary adenoma. has symptoms of headache and fatigue, visual changes, weakness, weight loss, muscle and soft tissue wasting, personality changes
HYPOPITUITARISM
Diseases of ANTERIOR PITUITARY ____ is a hyper secretion of growth hormone during adulthood*
Manifestations:
Enlargement of bones and face, hands and feet, protruding forehead and jaw.
Acromegaly
Diseases of the ANTERIOR PITUITARY
____ of ____
Caused by PROLACTINOMAS
Manifestations:
In Females: amenorrhea (no ovulations or periods) galactorrhea (milk secretion) hirsutism (hair growth) and osteopenia (bone loss)
In males: hypogonadism (small testes) and erectile dysfunction
Hypersecretion if PROLACTIN
DISEASES OF POSTERIOR PITUITARY
____ is hypersecretion of ADH
Causes: head trauma, circulatory damage
Manifestations: enhanced renal water retention, serum hyponatremia, serum hypo osmality, decreased urinary output, concentrated urine.
SIADH syndrome of inappropriate anti diuretic hormone secretion
___ is a hormone that increases collecting duct In the kidney nephron permeability to water, which increases absorption of water in the kidney which leads to dilutional hypoatremia
ADH
Diseases of the POSTERIOR PITUITARY
___ ___ is insufficiency of ADH- causing loss of too much water in urine.
Manifestation:
Polyuria, nocturia, continuous thirst
Diabetes insipidus
Diseases of POSTERIOR PITUITARY
TYPE OF DIABETES INSIPIDUS
__ insufficient secretion of ADH
Neurogenic (central)
Diseases of POSTERIOR PITUITARY
TYPE OF DIABETES INSIPIDUS
____ Is inadequate response of kidney tubules to ADH
Nephrogenic
Alterations of thyroid function
___ has a high T3 and T4, a low TSH and TRH.
Manifestations: like sympathetic NS stimulation, exothalamos-Bulging of the eyes, which causes the eyes to move out of the sockets in one or both eyes.
Hyperthyroidism
Alterations of thyroid function
has a high T3 and T4, a low TSH and TRH.
___ ___ is hyperthyroidism from TSH receptor antibodies, leads to nodular thyroid disease, eventually hypothyroidism
Treatment is thyroid destroying meds, surgery, iodine isotopes
Graves’ disease
Alterations of thyroid function
has a high T3 and T4, a low TSH and TRH.
__ ___ can lead to death within 48 hours without treatment.
Manifestations:
Fever, tachycardia, sweating, psychosis
Thyrotoxic crisis (thyroid storm)
Alterations of thyroid function
Deficient production of thyroid hormones T3, T4 by the thyroid.
___ ___ is a decreased T3 and T4, high TSH & TRH
Primary hypothyroidism
Alterations of thyroid function
___ ___ is the most common cause of primary hypothyroidism
Autoimmune disease causing gradual destruction of thyroid tissue.
Treatment: hormone replacement
Hashimoto disease
Hypothyroidism Low T3,T4 Low metabolic rate Present with endemic goiter Pale, cool, with edema. Cold intolerance No change with eyes Bradycardia, enlarged heart Lethargic, slow intellectual functions Some weight increase with decreased appetite
Hyperthyroidism High T3,T4 High metabolic rate Present goiter with Graves’ disease Flushed and warm Heat intolerance Exophthalmos with graves Tachycardia increased BP Restlessness, nervous, tremors Thin but increased appetite
Alterations of thyroid function
__ ___
Most common endocrine malignancy. Ionizing radiation most common cause.
Treatment with thyroidectomy, suppression therapy, radiation, and chemotherapy, hormone replacement
Thyroid carcinoma
Alterations of the parathyroid function
___ is increased secretion of parathyroid hormone.
Manifestations: hypercalcemia and hyperphosphatemia.
Hyperparathyroidism.
Alterations of the parathyroid function
Hyperparathyroidism is increased secretion of parathyroid hormone.
Manifestations: hypercalcemia and hyperphosphatemia.
___ is excess secretion of PTH from one or more parathyroid glands
Primary
Alterations of the parathyroid function
Hyperparathyroidism is increased secretion of parathyroid hormone.
Manifestations: hypercalcemia and hyperphosphatemia.
__ is increase in PTH secondary to chronic hypocalcemia
Secondary
Type ___ diabetes Mellitus has loss of beta cells, hyperglycemia when 80-90% of cells lost. Macrophages, T and B Lymphocytes and t natural killer cells are stimulated and result in beta cell destruction and apoptosis. Lack of insulin, amylin, excess glucagon lead to hyperglycemia.
Type 1
Type __ diabetes rages from INSULIN RESISTANCE with RELATIVE INSULIN DEFICIENCY to insulin secretory defect with insulin resistance and is caused by GENETIC ENVIORNMENTAL INTERACTION
Risk factors are ** age, obesity, hypertension, physical activity, and family history.
Metabolic syndrome
Type 2
Type ___ diabetes is the destruction of Beta cells related to genetic susceptibility and environmental factors.
Immunologically mediated destruction of beta cells
Manifestations
Hyperglycemia Polydipsia Polyuria Polyphagia Weight loss Fatigue
Type 1
Type __ diabetes manifestations:
Fatigue, recurrent infections, visual changes, neuropathy, weight loss, hyperinsulinemia
Type 2
Acute complications of diabetes mellitus
Hypoglycemia
Diabetic ketoacidosis
Hyperosmolar hyperglycemic non ketotic syndrome dangerous condition resulting from very high blood glucose levels. HHNS can affect both types of diabetics, yet it usually occurs amongst people with type 2 diabetes.
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____ _____ is onset over 4-10 hours. Lack of insulin, GI upset, Febrile illness. Breath has a fruity smell, kussmaul respiration’s, hypotension, thirsty, dehydration, high blood sugar, hyperkalemia,
Need to hydrate, insulin, electrolyte replacement
Diabetic ketoacidosis
Types of diabetes
___ __ ___ ___ beta cell function or insulin action affected by autosomal dominant mutations
Maturity onset diabetes of youth (MODY)
Type of diabetes
__ ___ ___ is any degree of glucose intolerance with onset or first recognition during pregnancy
Gestational diabetes mellitus (GDM)
Chronic complications of diabetes mellitus
TOXIC EFFECTS OF GLUCOSE
MACROVASCULAR DISEASE
INFECTIONS
HYPERGLYCEMIA
MICROVASCULAR DISEASE
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Disorder of adrenal cortex
___ disease is autoimmune of ADRENAL CORTEX
** not enough corticosteroid and mineral corticosteroid; need to ADD some more
Manifestations:
Bronze pigmentation of skin, changes in distribution of body hair, GI disturbances, weakness, weight loss, postural hypotension, hypoglycemia
Addison’s disease
Disorders of adrenal cortex
__ is high estrogens, development of female secondary sex characteristics
Feminization
___ is high androgens, development of male secondary sex characteristics
Virilization
Disorders or the adrenal medulla:
HYPER
adrenal medulla hyperfunction
Caused by tumors
Secrete CATECHOLAMINES on a continuous or episodic basis.
Pheochromocytoma (tumor)
Know
Lower bladder urinary tract obstruction types
Anatomical obstructions:
Enlarged prostate, prolapsed uterus, stricture or the urethra, low bladder wall compliance (stretch) blockage of urethra or lower bladder.
Symptoms: frequent voiding, nocturia, urgency, unable to empty, intermittent stream, poor force.
Overactive bladder syndrome
Contractions of bladder wall.
Symptoms: urgency, leaking, frequency crampy pain with no urinary tract infection.
Know
Normal bladder has a detrusor muscle contracting when bladder is full.
Overactive bladder is detrusor muscle contracting before bladder is full.
Know
Stages of urinary tract infection
- ___ is where pathogens colonizes the urethra and ascends towards the bladder
Colonization
Stages of UTI
- ___ is where pathogen penetrates bladder and bacteria replicates, potentially forming biofilms.
Uroepithelium penetrati
M
Stages of a UTI
- ___ is where bacteria ascends towards the kidneys via the ureters.
Ascension
Stages of UTI
- __ is where infection of the renal parenchyma causes an inflammatory response called pyelonephritis
Pyelonephritis
Stages of UTI
- __ ___ ___ is where bacteria continues to cascade up to the kidneys, leading to acute kidney injury
Acute kidney injury
___ __
Risk factors: urinary stasis due to (?)
Most common pathogens: e coli (bowel) and staphylococcus saprophyticus
Manifestations: frequency, urgency, dysuria, suprapubic and low back pain. RBC & WBC In urine.
Treatment is antibiotics hydration and avoid stasis.
Acute cystitis
__ __ is unpleasant sensation with lower urinary tract symptoms for more than 6 weeks with no infection or other causes.
Treatment; avoid triggers (foods), anti inflammatory meds, anti histamine, steroids.
Interstitial cystitis
__ ___ is infection of upper urinary tract (ureter, renal pelvis, and interstitium
Pathogens: E. coli, proteus, pseudomonas
Risk: cystitis, stasis/obstructions, general risk for infections (diabetes)
Manifestations: cystitis symptoms, plus fever, back pain, especially “CVAT”
Treatment: relieve stasis, antibiotics, hydration, pain meds, and fever reducers as needed.
Acute pyelonephritis. Oh
__ ___ persistent or recurring episodes of acute pyelonephritis that lead to scarring in one or both kidneys.
Chronic pyelonephritis
__ is a inflammation of the glomerulus, can be primary or secondary. Immune mechanisms are main component of primary and secondary injury.
Glomerulonephritis
Two major symptoms of glomerulonephritis if severe,
Hematuria with red blood cell casts.
Proteinuria exceeding 3-5 g/day with albumin (macroalbuminuria) as the major protein.
Know
__ ___ obstructs renal blood flow: decreased GFR, obstructs glomerular capillary blood flow and decreases GFR.
Loss of filtration barrier and escape of albumin.
Obstruction and loss of tubular reabsorption functions
Diabetic glomerulopathy
__ ___ is a characteristic of glomerulonephritis. Excretion if 3.5G or more of protein in urine per day. The protein excretion is caused by glomerular injury.
Findings: hypoalbuminemia, edema, hyperlipidemia, lipiduria, vitamin d deficiency, hypothyroidism
Nephrotic syndrome
Classification of kidney dysfunction
Renal insufficiency
Acute kidney injury
Kidney failure
End stage kidney disease
Know
___ ___ ___ is from renal insufficiency, kidney failure, and end stage kidney failure
Acute kidney injury
___ ___ __ is a sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood as demonstrated by an elevation in plasma creatinine and blood urea nitrogen BUN levels
Acute kidney injury
AKI-Pre renal.
Most common cause of AKI
Caused by impaired renal blood flow
Glomerular filtration rate (GFR) declines because of decrease in filtration pressure
Know how’s
____ is most commonly caused by acute tubular necrosis.
Intrarenal (intrinsic)
___ occurs with urinary tract obstructions that affect the kidneys BILATERALLY
Postrenal
AKI OLIGURIA
mechanisms: decrease in renal blood flow. Tubular obstruction, tubular backleak.
Duration depends on duration of ischemia and severity of injury.
Know
AKI PHASES AND RECOVERY
Initiation: kidney injury is evolving. Prevention of injury is possible.
Maintain oliguric: Established kidney injury: urine output is lowest
Serum creatinine and blood urea nitrogen both high
Recovery (polyuric) injury repaired and normal renal function reestablished. Diuresis is common. Decline in serum creatinine and urea. Increase in creatinine clearance.
Know
Chronic kidney disease
5 stages
Normal: (GFR>90 ml/min)
Mild (GFR 60-89 ml/min)
Moderate: (GFR 30-59 ml/min)
Severe: (GFR: 15-29 ml/min)
End stage: (GFR less than 15)
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CKD progression.
Factors in advanced renal disease:
Proteinuria & angiotensin II activity.
Poor creatinine and urea clearance from blood.
As GFR falls plasma creatinine increases.
Know
CKD effects on fluids and electrolyte balance.
Sodium and water balance: sodium excretion increases with obligatory water secretion leading to sodium deficit and volume loss. Kidneys ability to concentrate or dilute urine decreases.
Potassium: tubular secretion of K increases early lowering serum K. Once oliguria sets in, potassium retained; serum potassium goes UP.
Acid base balance: metabolic acidosis when GFR 20%-25% and can not secrete H+ of reabsorb bicarb
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3 affects of CKD
Calcium, phosphate, and bone Vitamin D.
Protein, CHO, fat metabolism change
Anemia (low hematopoietin)
Know
CKD MANIFESTATIONS
alterations seen in all systems
Cardiovascular Pulmonary Hematologic Immune Neurologic Gastrointestinal Endocrine and reproduction Integumentary
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__ ___ called nephrolithiasis, calculi, or urinary stones.
Risk factors: gender, age, race, geographic location, seasonal factors, fluid intake and diet: occupation. Genetic predisposition.
Classified by the minerals that make up the stone.
Kidney stones
Why do kidney stones form:
Supersaturation of one or more salts: presence of salt in a higher concentration with a fluid (urine) than the volume is able to dissolve to maintain equilibrium.
Precipitation of a salt from liquid to solid state:
Temperature and pH of urine. An alkaline urinary pH increases risk of stone formation.
Growth into a stone via crystallization or aggregation: crystals grow from a small nidus (nucleus) to larger stones in the presence of a super saturated urine
Know
Types of stones:
Calcium oxalate or calcium phosphate 70-80%- calcium oxalate
Struvite stones- 15% infection
Uric acid stones 7%
Know
Kidney stones:
Manifestations: renal colic; pain related to dilation and spasms
Evaluation: history, stone and urine analysis 24-hour urine, strain all urine. Imaging.
Treatment: high fluid intake. Decrease dietary intake of stone forming substances. Stone removal.
Know
Neuro anatomy of pain:
Nociception: activation of pain perception.
Nociceptors: free nerve endings in skin, muscles, joints, arteries, and viscera. Detect wide range of stimuli: chemical, mechanical, thermal. Two types of nerve fibers to spinal cord: a delta myelinated fibers (new, localized, and fast.)
Unmyelinated C polymodal fibers (old, diffuse, and slow)
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Sequence of pain perfection
Transduction: activation of nociceptors.
Transmission: nerve fiber conduction to dorsal horn and up spinal cord.
Perception: interpretation in the brain
Modulation: facilitation or inhibition of transmission before, during, or after perception
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Mechanisms of pain:
___ properly functioning nervous system sends signals that tissues are damaged requiring attention and care.
Nociceptive
Mechanisms of pain
___ damaged or malfunctioning nerves, also called pathological pain.
Neuropathic
Mechanisms of pain
Nociceptive: somatic (body pain) and visceral (gut) pain.
Neuropathic: peripheral neuropathies and central neuropathic pain.
Know
How to describe pain:
Pain threshold: point at which stimulus is perceived as pain.
Perceptual dominance: pain at one location may cause an increase in pain threshold in another location.
Pain tolerance: duration of time or the intensity of pain that a person will endure before initiation of pain responses
Know
__ __
Protective mechanism- alerts to a condition or experience that is immediately harmful.
Transient
Begins suddenly
Relieved after pain stimulus removed.
Acute pain
___ pain is from skin, joints, muscles. A-delta fibers: sharp and well localized. C-fibers: dull, aching,. Poorly localized
Somatic pain
__ pain is internal organs and lining of body cavities.
C fibers: poorly localized, aching, gnawing, throbbing, or intermittent cramping quality:
Often radiates or is referred
Visceral pain
Acute pain- REFFERRED
pain felt distant from its point of origin
Area of referred pain is supplied by the same spinal segment as site or origin
Know
___ pain is constant or intermittent. Sudden onset, or develops insidiously. Lasts at least 3-6 months. Response patterns very. Significant behavior and psychologic changes. Do NOT see psychologic signs like acute pain.
Chronic painless
Temp varies in response to
Location Activity Environment Circadian rhythm Gender Age
Know
Temperature regulation
Peripheral and central thermoreceptors, hypothalamic control, heat protection and conservation.
Chemical reactions of metabolism, skeletal muscle contractions, chemical thermogenesis, vasoconstriction, shivering, voluntary mechanisms
Knowi
Heat loss
Radiation Conduction Convection Evaporation Vasodilation Decreased muscle tone Increased respiration’s Voluntary measures Adaptation to warmer climates
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Age and temperature
Infants: produce sufficient body heat but are unable to conserve heat produced.
Small body size and high body surface to weight ratio. Thin subcutaneous layer.
Elderly: slow blood circulation, vasoconstrictive response, and decreased metabolic rate. Decreased sweating, shivering, and perception of heat and cold
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Fever:
Temporary resetting of the hypothalamic thermostat.
Active heat production and conservation measures to a new sent point
Exogenous pyrogens
Endogenous pyrogens
Fever of unknown origin
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Benefit of fever
Kills many micro organisms. Decrease serum levels of iron, zinc, and copper needed by germs.
Promotes lysosomal breakdown and auto destruction of cells
Increases lymphocytic transformation and phagocyte motility
Increases antiviral interferon production and phagocytosis
Know
__. Is elevation of the body temperature without an increase in the hypothalamic set point. Can produce nerve endings, coagulation or cell proteins, and death.
Many be therapeutic, accidental, or associated with stroke or heat trauma.
Hyperthermia
