Final Patho Exam Flashcards

(109 cards)

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
Canidate for Dialysis
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
26
GERD
Lower Esophageal sphincter dysfunction. gastric acid to backflow into esophagus
27
Hiatal Hernia
Contributes to GERD - disrupts normal barrier between esophagus and stomach.
28
Esophageal motility disorders
impaired peristalsis and reduces esophageal clearance = pooling of acid in esophagus. Ex CVA
29
GERD assessment
Heartburn, regurgitation and chest pain normal assessment unless esophagitis
30
Diagnostic tests for GERD
EGD, esophageal ph probe and esophageal manometry
31
Treatment of GERD
Diet management, lifestyle modification, antacids, H2 receptor antagonists, prokinetic agents PPIs X 6 weeks - then surgery
32
Warning signs of GERD
Over age of 50 y.o - Dysphagia, odynophagia, N/V/Weight loss/Melena. early satiety
33
Diagnosis of Hiatal Hernia
Diaphragmatic becomes weak = sliding hernia
34
Contributing factors to HH
Aging, obesity, PG, increased abdominal pressure (coughing/straining) or structural abnormalities
35
Symptoms of HH
GERD symptoms
36
Treatment of HH
Same as GERD
37
Duodenal Ulcer caused by
H.Pylori
38
Duodenal Ulcer patho
Gastric acid hypersecretion/impaired mucosal defense mechanism/disruption of balance between aggressive and defensive factors. (NSAIDS)
39
Duodenal Ulcer symptoms
chronic intermitted epigastric pain - appears 30 min 2 hours after eating (stomach empty) pain in the middle of night and gone in am.
40
Diagnosis of Duodenal Ulcer
Upper GI, H. Pylori testing, imaging
41
Treatment of Duodenal Ulcers
PPI, H2 receptors blockers, antibiotics for h. Pylori, antacids and cytoprotective agents lifestyle modifications
42
Peptic ulcer disease
Break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. (less likely in the large intestine)
43
Peptic ulcer patho
H/Pylori, NSAIDS, Lifestyle choices (ETOH/Drugs/smoking) gastric acid hypersecretions
44
Body's protective mechanisms for PUD
naturally secrete Mucus and bicarb secretions, prostaglandins, mucosal blood flow, epithelial cell renewal
45
Diagnose PUD
Endoscopy, H. pylori testing. imaging studies
46
Treatment of PUD
PPI, H2 receptors blockers, antibiotics for h. Pylori, antacids and cytoprotective agents lifestyle modifications. NO NSAIDS/ETOH/SMOKING. Dietary mods
47
Major Depressive Disorder (MDD) patho/transmitters
Neurotransmitter imbalance - serotonin -norepinephrine - Dopamine
48
Major Depressive Disorder (MDD) patho
Neurotransmitter imbalance Neuroendocrine dysregulation/abnormality in the hypothalamic-pituitary adrenal axis - elevated cortisol levels inflammatory process- chronic inflammation neuroplasticity and structure changes
49
First line treatment MDD
SSRIs look at age, side effects, safety and cost
50
Social Anxiety Disorder - Key factors
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
Can antiseizure meds be used for panic disorders
yes
52
Panic disorder
intense fear: 4 of 13 symptoms
53
Schizophrenia - positive symptoms
hallucinations, delusions, formal thought disorder, and bizarre behavior
54
Schizophrenia -negative symptoms
flattened affect, alogia, anhedonia, attention deficits, and apathy. Cognitive symptoms are the inability to perform daily tasks requiring attention and planning.
55
Schizophrenia diagnosis - neuroimaging
A consistent finding is the enlargement of the lateral and third ventricles and the widening of frontocortical fissures and sulci
56
Hypothyroidism
0.1-0.1% population, more common in women
57
Most common thyroid condition
Hypothyroidism
58
hypothalamic-pituitary axis
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
Hyperthyroidism disease
Graves' disease
60
Graves' Disease
everything enhanced, hyperactive of ANS that effects eye movement and eye lids
61
functional abnormalities/Graves disease/ ophthalmopathy
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
infiltrative changes /Graves disease/ ophthalmopathy
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
The two most distinguishing factors of Grave's disease
pretibial mxyedema and exophthalmos
64
hyperthyroidism treatment
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
goal of radioactive iodine ablation for the treatment of Graves disease
destroy the overactive thyroid tissue
66
Hypothyroidism
hormone replace therapy = levothyroxine
67
DM1- environmental factors that can cause
Viral infections, particularly enteroviruses, coxsackievirus, other infectious microorganisms Helicobacter pylori exposure to cow's milk proteins; lack of vitamin D
68
Diagnostic criteria for diabetes
according to the American Diabetes Association is: Hemoglobin A1C greater than or equal to 6.5% - 5.6-6.4 - prediabetes
69
Actions of insulin
insulin promotes glucose uptake mostly in the liver, muscle and adipose tissue
70
neuropathy complication of DM
Autonomic neuropathy includes/slows everything down: gastrointestinal symptoms: decreased esophageal motility, gastroparesis delayed gastric emptying
71
Hypoglycemic- Neurogenic reactions
occur when the decrease in blood glucose level is rapid and presents with: Tachycardia Palpitations Diaphoresis Tremors Pallor Arousal anxiety
72
Primary hyperparathyroidism
usually caused by parathyroid gland tumor. hypercalcemia
73
Adrenal tumors
Produces cortisol independent of the normal regulatory mechanisms of the HPA axis. Inc cortisol suppresses ACTH
74
Secondary hyperparathyroidism
increased PTH secretion in response to hypocalcemia Is usually caused by CKD As PTH increases, it can lead to hypercalcemia
75
Hypercalcemia
Hypercalcemia and hypophosphatemia (also due to hyperparathyroidism)
76
low bone density with hypocalcemia is seen
have low bone density (osteoporosis) that is most noted in the distal one-third of the radius
77
Complications of hypercalcemia
kidney stones, pathological fractures, ventricular hypertrophy, depression, gastric issues, osteoporosis, patho fractures. V-tach
78
Hypoparathyroidism labs
low Mag, inhibits PTH secretion and cause hypoparathyroidism Low Ca. High phosphate
79
Hypomagnesiumia in Hypoparathyroidism
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
Symptoms of hypocalcemia include
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
Hypercortisolism usually caused by
Adrenal tumors
82
Hypercortisolism - patho
Suppression of ACTH: due to high cortisol levels that exert negative feedback on the pituitary gland and hypothalamus which inhibits secretion of ACTH
83
Glucose intolerance is associated with
with hypercortisolism
84
Cushing's disease
Hypercortisolism - Pituitary tumors (Cushing’s disease): hypercortisolism caused by a pituitary tumor that secretes excess ACTH
85
Glucose intolerance is associated with hypercortisolism
intolerance occurs because of cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by the liver.
86
Cushing's syndrome
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
Hypocortisolism-Adrenal Crisis
Insufficient cortisol Lack of aldosterone Stress response failure Fluid and electrolyte imbalances
88
Adrenal crisis triggers
Infection Surgery Trauma Sudden discontinuation of corticosteroid therapy
89
Adrenal Crisis-Hypocortisolism
Hypotension/complete vascular collapse develops with undiagnosed disease, acute withdrawal of glucocorticoid therapy, or the occurrence of infection or other comorbid stressful events
90
Labs for Primary Hypocortisolism-Adrenal Insufficiency
Serum and urine levels of cortisol are depressed with primary hypocortisolism, and ACTH levels are increased.
91
Alzheimers
Decreased short-term memory occurs with mild cognitive decline as a result of a reduced hippocampus size.
92
Patho - Alzheimer's
Amyloid beta plaques, neurofibrillary tangles, neurotransmitter imbalance, inflammation, and vascular changes
93
Parkinson's disease symptoms
Symptoms associated with bradykinesia is shuffling gait Other classic symptoms include: Resting tremor, rigidity, postural disturbance, dysarthria, dysphagia
94
non=motor symptoms of parkinsons
Mood, Sleep, cognitive, autonomic, speech, swallowing and fatigue
95
MS
Demyelinating disease
96
MS risk factors
include smoking, vitamin D deficiency, and Epstein-Barr virus infection.
97
Patho of MS
Immune system dysfunction inflammation and demyelination axonal and neurodegeneration reactive gliosis remyelination attempts
98
Febrile seizures
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
Migraine Headache
Unilateral. episodic neurologic disorder whose marker is headache lasting 4 to 72 hours. throbbing pain, pain worsens with activity. N V
100
Cluster HA
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
Tension HA
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
Bell’s Palsy
associated with Cranial nerve VII paralysis and results in facial asymmetry and inability to close eye, smile or frown on the affected side
103
Trigeminal neuralgia
associated with compression of Cranial nerve V and results in severe and sharp stabbing pain that can worsen with chewing
104
Bacterial Meningitis
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
CVA: Infarct in the ACA will result in Motor:
contralateral paralysis or paresis (greater in foot and thigh)
106
Sensory deficits associated with a basilar artery infarct
contralateral loss of vibratory sense, sense of position with dysmetria, loss of two-point discrimination, impaired rapid alternating movements
107
Rosacea
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
Melanoma
most aggressive skin cancer; the thickness of the lesion impacts prognosis
109
Plaque Psoriasis
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