Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NUR507 Midterm > Final Patho Exam > Flashcards

Final Patho Exam Flashcards

1
Q

Acute Renal Failure

A

Reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Predictor of good prognosis in acute renal failure

A

Response to lasix

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

AKI

A

caused by ischemia - sudden and often reversible decline in kidney function. The reduced blood supply compromises the kidneys’ ability to filter waste products, maintain electrolyte balance, and regulate fluid volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cause of renal HTN

A

Ischemia activates the renin-angiotensin-aldosterone system (RAAS), a hormonal system that regulates blood pressure and fluid balance. The activation of RAAS can lead to vasoconstriction and increased retention of sodium and water, further contributing to fluid imbalance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ATN

A

Prolonged and severe ischemia can lead to tubular necrosis, a condition where renal tubular cells undergo cell death. Tubular necrosis is a critical factor in the development of acute kidney injury.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Stages of ARF

A

oliguric, diuretic and recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ARF labs

A

increase of baseline Cr >50%
decrease in Cr clearance more tham 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Types of ARC

A

Pre-renal, intrarenal, and post Renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pre-renal

A

most common. before the kidney. dehydration/hypoperfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Intrarenal (structural)

A

process that damages kidney. ATN, Glomerulonephritis, nephritis, rhabdo, tumor lysis, meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Post renal ARF

A

Caused by disease states located downstream of the kidney. urinary obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment of ARF

A

immediately treat pul edema or hyperkalemia. remove cause. dialysis. restrict Na, H2O & K
phosphate binders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chronic Renal failure

A

progressive/irreversible
GFR < 60 for 3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Stages of CRF

A

1- GFR normal/kidney damage/proteinuria
2- GFR 60-88
3- GFR 30-59
4- GFR 15-29
5 GFR less than 15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of CRF

A

Glomerulonephritis (most common)
DM (most significant risk factor)
HTN
Tubulointersitial nephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute pyelonephritis patho

A

Bacterial colonization, adherence and invasion
Inflammation and immune response
renal injury and complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diagnosis Pyelonephritis

A

Difficult to diagnose/similar to cystitis
involves upper tract of renal tract
Flank pain, fever, abd tenderness, chills, tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cystitis

A

involves the lower urinary tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Diagnostics for Pyelo

A

UA- bacteria, pyuria, possible WBC casts
CBC - indicate infection
Imaging - renal US or CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Treatment of Pyelo

A

Antibiotics/hospitalization/IVFs/follow up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Renal Calculi - type of ARF

A

Can cause post renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Renal Calculi patho

A

Supersaturation: with substances like Ca
Nucleation: crystals cause nucleation sites = more deposits of Ca
Crystal Retention: urinary stasis/inadequate urine flow
Stone growth: crystals form stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Physical exam with Renal calculi

A

Hematuria, flank pain, CVA tenderness
CT - presence of stone/size/location
look for renal failure with BUN/Cr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Treatment of Renal Calculi

A

Based on size: 5 mm or less pass on own/mild symptoms
Greater than 5mm - lithotripsy, pain management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Canidate for Dialysis

A

Symptomatic uric acid, acute renal failure trying to recover. based more on the patient’s symptoms than the GFR. Fluid overload and HTN. Hypokalemia. acid/base imbalances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

GERD

A

Lower Esophageal sphincter dysfunction. gastric acid to backflow into esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Hiatal Hernia

A

Contributes to GERD - disrupts normal barrier between esophagus and stomach.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Esophageal motility disorders

A

impaired peristalsis and reduces esophageal clearance = pooling of acid in esophagus. Ex CVA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

GERD assessment

A

Heartburn, regurgitation and chest pain
normal assessment unless esophagitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Diagnostic tests for GERD

A

EGD, esophageal ph probe and esophageal manometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Treatment of GERD

A

Diet management, lifestyle modification, antacids, H2 receptor antagonists, prokinetic agents PPIs X 6 weeks - then surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Warning signs of GERD

A

Over age of 50 y.o
- Dysphagia, odynophagia, N/V/Weight loss/Melena. early satiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diagnosis of Hiatal Hernia

A

Diaphragmatic becomes weak = sliding hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Contributing factors to HH

A

Aging, obesity, PG, increased abdominal pressure (coughing/straining) or structural abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Symptoms of HH

A

GERD symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Treatment of HH

A

Same as GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Duodenal Ulcer caused by

A

H.Pylori

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Duodenal Ulcer patho

A

Gastric acid hypersecretion/impaired mucosal defense mechanism/disruption of balance between aggressive and defensive factors. (NSAIDS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Duodenal Ulcer symptoms

A

chronic intermitted epigastric pain - appears 30 min 2 hours after eating (stomach empty) pain in the middle of night and gone in am.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Diagnosis of Duodenal Ulcer

A

Upper GI, H. Pylori testing, imaging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Treatment of Duodenal Ulcers

A

PPI, H2 receptors blockers, antibiotics for h. Pylori, antacids and cytoprotective agents
lifestyle modifications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Peptic ulcer disease

A

Break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. (less likely in the large intestine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Peptic ulcer patho

A

H/Pylori, NSAIDS, Lifestyle choices (ETOH/Drugs/smoking) gastric acid hypersecretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Body’s protective mechanisms for PUD

A

naturally secrete Mucus and bicarb secretions, prostaglandins, mucosal blood flow, epithelial cell renewal

45
Q

Diagnose PUD

A

Endoscopy, H. pylori testing. imaging studies

46
Q

Treatment of PUD

A

PPI, H2 receptors blockers, antibiotics for h. Pylori, antacids and cytoprotective agents
lifestyle modifications. NO NSAIDS/ETOH/SMOKING. Dietary mods

47
Q

Major Depressive Disorder (MDD) patho/transmitters

A

Neurotransmitter imbalance
- serotonin
-norepinephrine
- Dopamine

48
Q

Major Depressive Disorder (MDD) patho

A

Neurotransmitter imbalance

Neuroendocrine dysregulation/abnormality in the hypothalamic-pituitary adrenal axis - elevated cortisol levels

inflammatory process- chronic inflammation

neuroplasticity and structure changes

49
Q

First line treatment MDD

A

SSRIs
look at age, side effects, safety and cost

50
Q

Social Anxiety Disorder - Key factors

A

fear and avoidance of social situations.
For example, the anxious person may feel very uncomfortable having a conversation or interacting with others and very conscious of being scrutinized and humiliated or rejected by others.

51
Q

Can antiseizure meds be used for panic disorders

A

yes

52
Q

Panic disorder

A

intense fear: 4 of 13 symptoms

53
Q

Schizophrenia - positive symptoms

A

hallucinations, delusions, formal thought disorder, and bizarre behavior

54
Q

Schizophrenia -negative symptoms

A

flattened affect, alogia, anhedonia, attention deficits, and apathy. Cognitive symptoms are the inability to perform daily tasks requiring attention and planning.

55
Q

Schizophrenia diagnosis - neuroimaging

A

A consistent finding is the enlargement of the lateral and third ventricles and the widening of frontocortical fissures and sulci

56
Q

Hypothyroidism

A

0.1-0.1% population, more common in women

57
Q

Most common thyroid condition

A

Hypothyroidism

58
Q

hypothalamic-pituitary axis

A

hypothalamus releases thyroid releasing hormone = causes release by anterior pituitary gland stimulate TSH that goes to thyroid gland to stimulate T4 and T3 stimulated

59
Q

Hyperthyroidism disease

A

Graves’ disease

60
Q

Graves’ Disease

A

everything enhanced, hyperactive of ANS that effects eye movement and eye lids

61
Q

functional abnormalities/Graves disease/ ophthalmopathy

A

functional abnormalities resulting from hyperactivity of the sympathetic division of the autonomic nervous system (lag of the globe on upward gaze or a lag of the upper lid on downward gaze)

62
Q

infiltrative changes /Graves disease/ ophthalmopathy

A

involving the orbital contents with enlargement of the ocular muscles. These changes affect more than half of individuals with Graves disease. Increased secretion of hyaluronic acid, adipogenesis, inflammation, and edema of the orbital contents result in exophthalmos (protrusion of the eyeball), periorbital edema, and extraocular muscle weakness leading to strabismus and diplopia (double vision).

63
Q

The two most distinguishing factors of Grave’s disease

A

pretibial mxyedema and exophthalmos

64
Q

hyperthyroidism treatment

A

Treatment is directed at controlling excessive TH production, secretion, or action and includes antithyroid drug therapy (methimazole or propylthiouracil), radioactive iodine therapy (absorbed only by thyroid tissue, causing death of cells), and surgery.

65
Q

goal of radioactive iodine ablation for the treatment of Graves disease

A

destroy the overactive thyroid tissue

66
Q

Hypothyroidism

A

hormone replace therapy = levothyroxine

67
Q

DM1- environmental factors that can cause

A

Viral infections, particularly enteroviruses, coxsackievirus, other infectious microorganisms
Helicobacter pylori
exposure to cow’s milk proteins;
lack of vitamin D

68
Q

Diagnostic criteria for diabetes

A

according to the American Diabetes Association is: Hemoglobin A1C greater than or equal to 6.5%

  • 5.6-6.4 - prediabetes
69
Q

Actions of insulin

A

insulin promotes glucose uptake mostly in the liver, muscle and adipose tissue

70
Q

neuropathy complication of DM

A

Autonomic neuropathy includes/slows everything down:
gastrointestinal symptoms:
decreased esophageal motility,
gastroparesis
delayed gastric emptying

71
Q

Hypoglycemic- Neurogenic reactions

A

occur when the decrease in blood glucose level is rapid and presents with:
Tachycardia
Palpitations
Diaphoresis
Tremors
Pallor
Arousal anxiety

72
Q

Primary hyperparathyroidism

A

usually caused by parathyroid gland tumor.
hypercalcemia

73
Q

Adrenal tumors

A

Produces cortisol independent of the normal regulatory mechanisms of the HPA axis. Inc cortisol suppresses ACTH

74
Q

Secondary hyperparathyroidism

A

increased PTH secretion in response to hypocalcemia
Is usually caused by CKD
As PTH increases, it can lead to hypercalcemia

75
Q

Hypercalcemia

A

Hypercalcemia and hypophosphatemia (also due to hyperparathyroidism)

76
Q

low bone density with hypocalcemia is seen

A

have low bone density (osteoporosis) that is most noted in the distal one-third of the radius

77
Q

Complications of hypercalcemia

A

kidney stones, pathological fractures, ventricular hypertrophy, depression, gastric issues, osteoporosis, patho fractures. V-tach

78
Q

Hypoparathyroidism labs

A

low Mag, inhibits PTH secretion and cause hypoparathyroidism
Low Ca. High phosphate

79
Q

Hypomagnesiumia in Hypoparathyroidism

A

may be related to chronic alcoholism, malnutrition, malabsorption, increased renal clearance of magnesium caused by the use of aminoglycoside antibiotics or certain chemotherapeutic agents, or prolonged magnesium-deficient parenteral nutritional therapy.

80
Q

Symptoms of hypocalcemia include

A

Dry skin
Loss of body and scalp hair
Hypoplasia of developing teeth
Horizontal ridges on the nails
Cataracts
Basal ganglia calcifications
Bone deformities
Bowing of the long bones

81
Q

Hypercortisolism usually caused by

A

Adrenal tumors

82
Q

Hypercortisolism - patho

A

Suppression of ACTH: due to high cortisol levels that exert negative feedback on the pituitary gland and hypothalamus which inhibits secretion of ACTH

83
Q

Glucose intolerance is associated with

A

with hypercortisolism

84
Q

Cushing’s disease

A

Hypercortisolism - Pituitary tumors (Cushing’s disease): hypercortisolism caused by a pituitary tumor that secretes excess ACTH

85
Q

Glucose intolerance is associated with hypercortisolism

A

intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver.

86
Q

Cushing’s syndrome

A

too much cortisol. characterized by patterns of fat deposition have been described as “truncal [central] obesity,” “moon face,” and “buffalo hump. arms and legs thin

87
Q

Hypocortisolism-Adrenal Crisis

A

Insufficient cortisol
Lack of aldosterone
Stress response failure
Fluid and electrolyte imbalances

88
Q

Adrenal crisis triggers

A

Infection
Surgery
Trauma
Sudden discontinuation of corticosteroid therapy

89
Q

Adrenal Crisis-Hypocortisolism

A

Hypotension/complete vascular collapse

develops with undiagnosed disease, acute withdrawal of glucocorticoid therapy, or the occurrence of infection or other comorbid stressful events

90
Q

Labs for Primary Hypocortisolism-Adrenal Insufficiency

A

Serum and urine levels of cortisol are depressed with primary hypocortisolism, and ACTH levels are increased.

91
Q

Alzheimers

A

Decreased short-term memory occurs with mild cognitive decline as a result of a reduced hippocampus size.

92
Q

Patho - Alzheimer’s

A

Amyloid beta plaques, neurofibrillary tangles, neurotransmitter imbalance, inflammation, and vascular changes

93
Q

Parkinson’s disease symptoms

A

Symptoms associated with bradykinesia is shuffling gait
Other classic symptoms include:
Resting tremor, rigidity, postural disturbance, dysarthria, dysphagia

94
Q

non=motor symptoms of parkinsons

A

Mood, Sleep, cognitive, autonomic, speech, swallowing and fatigue

95
Q

MS

A

Demyelinating disease

96
Q

MS risk factors

A

include smoking, vitamin D deficiency, and Epstein-Barr virus infection.

97
Q

Patho of MS

A

Immune system dysfunction
inflammation and demyelination
axonal and neurodegeneration
reactive gliosis
remyelination attempts

98
Q

Febrile seizures

A

One possibility for the development of febrile seizures is that neurons are excited by decreased CO2 levels caused by hyperventilation during a febrile state

increased metabolism = increased RR = blow off CO2 = seizure

99
Q

Migraine Headache

A

Unilateral. episodic neurologic disorder whose marker is headache lasting 4 to 72 hours. throbbing pain, pain worsens with activity. N V

100
Q

Cluster HA

A

unilateral trigeminal distribution of severe pain with ipsilateral autonomic manifestations, including tearing on the affected side, ptosis of the ipsilateral eye, and congestion of the nasal mucosa. more in men 20-50.

Midface/teeth pain

101
Q

Tension HA

A

most prevalent type of recurrent headache. It is not a vascular or migrainous headache. The average age of onset is during the second decade of life. It is usually a mild to moderate bilateral headache with a sensation of a tight band or pressure around the head.

Tight band or pressure around head

102
Q

Bell’s Palsy

A

associated with Cranial nerve VII paralysis and results in facial asymmetry and inability to close eye, smile or frown on the affected side

103
Q

Trigeminal neuralgia

A

associated with compression of Cranial nerve V and results in severe and sharp stabbing pain that can worsen with chewing

104
Q

Bacterial Meningitis

A

include fever, tachycardia, and chills. The clinical manifestations of meningeal irritation are a severe throbbing headache, severe photophobia, nuchal rigidity, and positive Kernig and Brudzinski signs

105
Q

CVA: Infarct in the ACA will result in Motor:

A

contralateral paralysis or paresis (greater in foot and thigh)

106
Q

Sensory deficits associated with a basilar artery infarct

A

contralateral loss of vibratory sense, sense of position with dysmetria, loss of two-point discrimination, impaired rapid alternating movements

107
Q

Rosacea

A

familial tendency, and several genes have been identified. Neurovascular dysregulation, infection, and factors that trigger altered innate and adaptive immune response are involved (i.e., chronic sun exposure and damage, heat, drinking alcohol or hot beverages, hormonal fluctuations, Demodex folliculorum [mites] colonization, and mental stress and anxiety).

108
Q

Melanoma

A

most aggressive skin cancer; the thickness of the lesion impacts prognosis

109
Q

Plaque Psoriasis

A

typical lesion of plaque psoriasis is a well-demarcated, thick, silvery, scaly, erythematous plaque surrounded by normal skin that can appear anywhere on the body

NUR507 Midterm (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions