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Nursing school level 2 > patho test #1 > Flashcards

patho test #1 Flashcards

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1
Q

pain pathway

A

afferent - brain interprets - efferent

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2
Q

A-delta

A

fat and purposeful - acute pain that helps us from gettin g hurt

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3
Q

c-fiber

A

slower- chronic pain - ongoing or intermittent

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4
Q

pain facilitators

A

glutamate, substance P, histamine, prostaglandin, bradykinin

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5
Q

pain inhibitors

A

opioids, GABA, cannabinoids, serotonin, norepinephrine

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6
Q

GABA is ______ when drinking

A

depressed

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7
Q

acute pain is a response from

A

the sympathetic nervous system

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8
Q

chronic pain

A

pain without a sympathetic response

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9
Q

impulses synapse at

A

dorsal horn

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10
Q

facilitators are also known as

A

excitatory

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11
Q

what do excitatory neurotransmitters do

A

increase sensitivity and responsiveness and respond to injury and inflammation

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12
Q

endogenous opioids

A

morphine like neuropeptides - mu, kappa, and delta

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13
Q

what do endogenous opioids do?

A

prevent opening of ion channels - slows pain response and digestion

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14
Q

patients on pain meds are usually constipated. what neurotransmitter causes that?

A

mu

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15
Q

endocannabinoids

A

phospholipids - modulate pain, sleep, immune function, appetite, and stress response

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16
Q

pain is

A

highly subjective

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17
Q

pain threshold

A

minimum stimuli needed to recognize pain. is similar amongst individuals

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18
Q

perceptual dominance

A

what’s bothering them the worst is what a patient will tell you about, but still do a full assessment incase there is something else wrong

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19
Q

what can increase pain threshold

A

sexual activity and acupuncture which increases neuromodulators

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20
Q

pain tolerance

A

the most amount of pain one can endure. varies among people and can vary depending on what the person is going through

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21
Q

what can lower pain tolerance

A

anger, anxiety, depression, isolation, chronic pain, tiredness

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22
Q

what can raise pain tolerance

A

diversion, rest, alcohol, medications, and culture

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23
Q

acute pain

A

sudden and responsive to treatment

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24
Q

acute on chronic

A

exacerbation of pain will take 20-40% more opioids

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25
Q

chronic pain

A

persistent and reoccurring. greater than 3 months, and resistant to pharmacological treatment

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26
Q

somatic pain

A

msk pain give NSAIDs

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27
Q

visceral

A

organ pain give opioids

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28
Q

opioid naive

A

either haven’t had them or haven’t had them in a really long time. exacerbated drug response and side effect due to lack of exposure to drug

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29
Q

opioid tolerant

A

adapted state of repeated drug exposure resulting in decreased efficacy of drug - it will be difficult to achieve desired response to pain

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30
Q

PCA

A

patient controlled analgesia

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31
Q

PCA by proxy

A

when someone else that is not the patient pushes the button - not good

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32
Q

ER vs IR

A

extended release and immediate release

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33
Q

breakthrough pain

A

severe pain that erupts while the patient is already medicated with a long acting painkiller - should use IV or IR for it

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34
Q

adjuvant

A

a agent that modifies the effect of other agents - used to decrease the amount of opioids used

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35
Q

examples of adjuvants

A

NSAIDs, antidepressants, anti epileptics, corticosteroids

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36
Q

sign of opioid withdrawal

A

N/V, HTN, tachycardia, pain, sometimes seizures

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37
Q

number one cause of acute kidney injury

A

sepsis because of decrease percussion to the kidney

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38
Q

oliguria vs anuria

A

oliguria - under 400 mL urine per day

anuria - without urine

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39
Q

causes of acute kidney injury

A

sepsis, ischemic injury, and toxic injury

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40
Q

kidney labs during acute kidney injury

A

increased creatinine, increased BUN, decrease GFR

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41
Q

can acute kidney injury be reversed

A

yes

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42
Q

what does acute kidney injury cause

A

inflammatory response, vascular response, and cell death

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43
Q

signs of acute kidney injury

A

hyperkalemia, hypermagnesemia, hyperphosphatemia, metabolic acidosis

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44
Q

uremia vs azotemia

A

uremia - a syndrome of renal failure and includes elevated blood urea and creatinine levels accompanied by fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes
azotemia - characterized by increased blood urea nitrogen levels and frequently increased serum creatinine levels. Renal insufficiency or renal failure causes azotemia.

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45
Q

normal BUN level

A

8-20

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46
Q

normal creatinine

A

0.7-1.4

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47
Q

what happens when bodys compensates with H+

A

causes potassium to leave the cell and causes even more potential to have hyperkalemia

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48
Q

prerenal acute renal injury

A

involves the heart and decreased cardiac output not HTN this causes inadequate renal perfusion

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49
Q

causes of prerenal acute renal injury

A

hypovolemia/hypoperfusion, sepsis, cardiac insufficiency (decreased cardiac output), and arterial renal stenosis

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50
Q

how do you treat prerenal acute renal injury

A

identify cause and treat the cause and increase BP

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51
Q

what happens to GFR, renin, ADH, and NA/h2o during prerenal acute renal injury

A

decrease GFR and increased renin and ADH. Na and H2O retention

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52
Q

opioid overdose death usually from

A

respiratory depression

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53
Q

what would you be likely to see during an assessment of an opioid overdose

A

low RR

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54
Q

harmful AE from morphine

A

hypotension

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55
Q

what electrolyte can cause cardiac arrest if you give it too fast

A

potassium

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56
Q

wrong concentration of what electrolyte can put pt into acute exacerbation of heart failure

A

sodium

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57
Q

intrarenal acute kidney injury

A

problem inside the kidney

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58
Q

causes of intrarenal acute kidney injury

A

tubular necrosis caused by HTN, bilateral pyelonephritis, DIC, myoglobin, ischemia, toxicity

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59
Q

DIC

A

disseminated intravascular coagulation - is a condition in which blood clots form throughout the body, blocking small blood vessels

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60
Q

postrenal acute kidney injury

A

problems effecting the kidney after the kidney

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61
Q

what can cause postrenal acute kidney injury

A

bilateral obstruction - stones obstructing
BPH
neurogenic bladder - bladder not voiding on own

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62
Q

intrarenal acute kidney injury treatment

A

antibiotic to get rid of infection

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63
Q

goals for acute kidney injury

A

identify cause and prevent injury, fluid and electrolyte balance, BP regulation, prevent infection, make sure medications aren’t nephrotoxic

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64
Q

what can the progression of renal failure lead to

A

progressive cell death

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65
Q

what happens when the kidney is recovering

A

function is restored but cannot concentrate, polyuria with Na, H2O, and potassium loss, fluid and electrolyte imbalance

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66
Q

how long can kidney recovery take

A

3-12 months

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67
Q

examples of dietary sources of potassium

A

spinach, tuna, strawberry, cucumber, banana, avocado, mango

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68
Q

hypotonic

A

not enough salt in blood

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69
Q

hypertonic

A

too much salt in blood

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70
Q

1 body system effected by altered sodium level

A

brain

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71
Q

hypokalemia symptoms

A

irregular pulse and dysrythmias with flattened t and u waves, GI upset, and myalgias to paralysis with respiratory failure

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72
Q

myalgias

A

muscle aches

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73
Q

hyperkalemia

A

peaked Ts with widening QRS, myalgias, paralysis, GI upset

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74
Q

hyperkalemia treatment

A

sodium polystyrene sulfonate, calcium gluconate, IV insulin/dextrose, hemodialysis

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75
Q

calcium replacements

A

carbonate, gluconate, chloride

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76
Q

GFR

A

best lab for renal function - mL of blood per min though glomerulus

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77
Q

lab value for hydration

A

BUN - test for urea

78
Q

urinalysis with increased protein =

A

decreased renal function

79
Q

blood in urine =

A

renal stones

80
Q

top causes of chronic kidney disease

A

DM- uncontrolled hyperglycemia - causes glucose to stick to artery wall which cause damage to artery supplying blood to kidney
HTN (systemic), glomerulonephritis, lupus, chronic UTI

81
Q

who has higher risk of chronic kidney disease

A

geriatrics, African American, hispanics, Pacific Islanders, native Americans

82
Q

chronic kidney disease is defined by

A

GFR below 60 for over 3 months

83
Q

treatment of chronic kidney disease

A

identification, protection of remaining glomerular function, correct F&E imbalance supplementation, protein restriction, dialysis, and possible renal transplant

84
Q

what medications would you give to chronic kidney disease pt

A

Ace inhibitors/ARBs, glycemic control, antilipemics, make if patient is on nephrotoxic drugs that the benefit of giving the drug outweighs the risk, and supplementation with Ca, vitamin D, and iron

85
Q

why do you want to restrict protein in chronic kidney disease

A

so they have less protein destroying the endothelial layers

86
Q

epoetin alfa

A

Epoetin alfa is a man-made form of a protein that helps your body produce red blood cells

87
Q

platelet aggregation

A

the clumping together of platelets

88
Q

antipyretic

A

used to prevent or reduce fever

89
Q

osteoarthritis

A

degenerative, low grade inflammatory joint disease

90
Q

what can cause osteoarthritis

A

obesity, repetitive trauma on load bearing joints, or too much work on joints such as running

91
Q

what happens to joints during osteoarthritis

A

erosion of cartilage, thickening and inflammation of synovial capsule, osteophytosis, and pain with limited range of motion

92
Q

treatment for osteoarthritis

A

plain films which are a 2 dimensional picture and NSAIDs to cut out inflammatory response, exercise, weight loss, and assistive devices because joint stiffness decrease with movement

93
Q

osteophytosis

A

new bone formation of joint margins also called bone spurs

94
Q

when cartilage gets broken up the fragments are taken up by the cartilage cells and digested by

A

the cell’s own lysosomal enzymes

95
Q

what 2 things are thought to play a major role in cartilage degradation in osteoarthritis pt

A

proinflammatory cytokines - interleukin 1 and tumor necrosis factor

96
Q

gout

A

syndrome caused by either overproduction or under-excretion of uric acid and is characterized by inflammation and pain in the joints

97
Q

hyperuricemia

A

An excess of uric acid in the blood.

98
Q

what does uric acid do to tissues

A

crystallizes, forming insoluble precipitates that are deposited in connective tissues throughout the body.

99
Q

where are 50% of initial attacks of gout

A

on the big toe. will be swollen and red

100
Q

if you have gout what are you more likely to get

A

1000x more likely to get kidney stones

101
Q

treatment for gout

A

fluids - up to 3L/day, diet considerations, NSAIDs, allopurinol (zyloprim)

102
Q

diet considerations for gout pt

A

no beef, pork, organ meats, shellfish, or beer

103
Q

agranulocytosis

A

also known as granulopenia, is an acute condition involving a severe and dangerous leukopenia (lowered white blood cell count)

104
Q

aplastic anemia

A

condition that occurs when your body stops producing enough new blood cells

105
Q

osteoporosis

A

silent progressive bone loss in which pt has more bone resorption and new bone formation

106
Q

woman with osteoarthritis who are 50 or older have a ______ more risk for fracture compared to men who are at a

A

woman - 50%.

men - 20% factor risk in later years

107
Q

most common areas of fracture in osteoporosis pt

A

femur, wrist, and thoracic/lumbar spine

108
Q

advanced disease state in osteoporosis pt shows as

A

pain and bone deformity and can have kyphosis

109
Q

kyphosis

A

vertebral collapse

110
Q

postmenopausal induced osteoporosis

A

from estrogen deficiency which causes and abundance of RANKL and decrease influence of OPG, and more bone destroyers than bone formers

111
Q

what does OPG do

A

stops bone resorption

112
Q

glucocorticoid-induced osteoporosis

A

caused from taking corticosteroids which causes an increase of osteoclast survival, inhibits osteoblast formation, and decrease OPG production

113
Q

increase of osteoclast survival causes

A

longer periods of bone resorption

114
Q

fatal complications of hip fracture

A

fat embolus from lipids in the bone marrow, PNA, and hemorrhage. 24% of those with hip fracture die within the first year of injury

115
Q

identify the primary function of the renal system

A

maintain homeostasis by reabsorbing nutrients and conserving water

116
Q

where exactly in the kidney does blood filtration take place

A

at the glomerulus

117
Q

what is normal GFR

A

60 - 120 mL/min

118
Q

what do juxtaglomerular cells do

A

they regulate renal blood flow and systemic blood pressure by secreting renin

119
Q

what stimulate juxtaglomerular cells

A

macula dense cells stimulates them in response to low sodium

120
Q

2 natural (hormonal) antagonists to the RAA system

A

urodilatin and BNP

121
Q

urodilatin

A

hormone that causes natriuresis through increasing renal blood flow

122
Q

anti-diuretic hormone is released in response to

A

low blood volume and causes reabsorption of water

123
Q

the majority of the body’s water is typically located where?

A

in the intracellular space

124
Q

which fluid compartment is potassium found in larger amounts

A

potassium is found in larger amounts inside the cell

125
Q

unilateral leg swelling is seen in a patient with a DVT due to which net filtration abnormality

A

an increase in capillary hydrostatic pressure

126
Q

identify two abnormalities most likely seen on a ECG after a pt has a severe crush injury

A

prolonged PR interval and widened QRS

127
Q

aldosterone =

A

sodium retention

128
Q

when is BNP released and what 3 effects does it have on the body

A

BNP is released when there is too much sodium. It causes vasodilation, sodium and water excretion, and decrease in blood pressure.

129
Q

When are colloids indicated and WHY would they be a good choice for these indications?

A

Colloids are indicated in treatment of burns, hepatic failure, and CHF. Colloids are a good choice for these treatments because they bring the oncotic pressure within the vascular space back up and increase fluid volume by moving the fluid from the interstitial space back into the vascular space, which overall will help with the high fluid volume and edema that occur in these patients

130
Q

Describe what happens in the vascular space when hypertonic fluids are given.

A

Hypertonic solutions cause the concentration of the vascular space to increase by pulling the fluids from inside the cells into the plasma fluids. Patients are at an increased risk for volume overload with these solutions

131
Q

what would want to ask before giving IV fluids

A

questions about fluid volume overload

132
Q

function of red bone marrow

A

blood cell formation

133
Q

yellow bone marrow is primarily

A

fat

134
Q

what 2 things can an intraosseous catheter deliver to the bloodstream

A

medications and IV fluids

135
Q

name 2 reasons why RANKL is secreted by osteoblasts

A

To maintain quality when microfractures occur, or when minerals such as calcium or phosphate need to be released into the bloodstream

136
Q

RANKL

A

The interaction of RANK with its ligand (RANKL) has been identified as the final common pathway through which bone resorption is regulated

137
Q

identify 4 synovial joints

A

Hinge joint- knee, ball and socket joint- hip, pivotal joint- C1 (to move head around), and the joints in the hand and wrist

138
Q

why do synovial joints lose mobility and stability

A

When the fluid within the joint decreases or increases it causes the person pain and will decrease the mobility and stability of the joint. This can be caused by rheumatoid arthritis and other autoimmune disorders.

139
Q

when is creatinine released into the blood

A

Creatinine is a normal byproduct and is released into the blood stream due to skeletal muscle metabolism.

140
Q

elevated serum myoglobin indicates

A

injury to the muscle

141
Q

lactic acid is used as a marker for the

A

severity of sepsis

142
Q

what decreases the ability of RANKL to initiate bone resorption

A

estrogen

143
Q

why do people gain weight as they age when they don’t increase their caloric intake

A

muscle mass decreases at the rate of about a half of a pound per year, which decreases metabolism. This is the cause of the shift of people gaining weight without increasing their caloric intake after the age of 30

144
Q

chronic kidney disease is not apparent until

A

less than 25% function remains

145
Q

uremia

A

abnormally high waste amounts in blood

146
Q

GFR of kidney failure

A

below 15

147
Q

GFR of kidney disease

A

15-60

148
Q

rheumatoid arthritis

A

auto-immune condition that causes inflammation of the joints through the activation of synovial fibroblasts and immune response

149
Q

fibroblasts

A

any cell from which connective tissue is developed

150
Q

angiogenesis

A

physiological process through which new blood vessels form from pre-existing vessels

151
Q

how is rheumatoid arthritis diagnosed

A

rheumatoid factor (autoantibodies) which is detectable in the blood

152
Q

stages of rheumatoid arthritis

A
  1. Inflammation of synovium - T and B cell and neutrophil infiltration into synovium which causes inflammation and some loss of mobility
  2. Formation of pannus and angiogenesis - layer of vascular fibrous tissue - will damage bone and cartilage due to RANKL activation
  3. Space within the joint will disappear and erosion of joint and supporting ligaments and tendons
  4. Bony ankylosis - bones will fuse together - cause stiffness and immobility of joint
153
Q

extrasynovial nodules

A

inflammatory cells surrounding cellular debris. happens in rheumatoid arthritis and can occur in the subcutaneous tissue, lungs, heart, or eyes

154
Q

what is urea

A

waste product produced from liver breaking down protein

155
Q

if you have decreased GFR what happened in the body

A

decreased urine output, increased fluid, increased waste in blood, and electrolyte imbalance - body will becomes acidic and go into metabolic acidosis

156
Q

How can myoglobin cause infrarenal injury?

A

excess myoglobin may thus cause renal tubular obstruction, direct nephrotoxicity (ischemia and tubular injury), intrarenal vasoconstriction

157
Q

how can sepsis lead to kidney injury

A

blood pressure drops dangerously low, affecting how the blood flows through your body. Because the blood can’t flow as quickly as it should, it can’t deliver the nutrients needed by the body’s tissues and organs. At the same time, the blood begins to clot within the blood vessels (called disseminated intravascular coagulation, or DIC), slowing down blood flow even more.

158
Q

Intact nephron hypothesis

A

loss of nephron mass with progressive kidney damage causes surviving nephrons to sustain normal kidney function – compensation for loss - beginning of CKD

159
Q

tubulointerstitial fibrosis

A

injury to the tubule and capillary leads to generation of chemotactic and adhesive factors that result in macrophage and T-cell accumulation

160
Q

why does chronic kidney disease cause bone pain

A
  • Kidneys activate vitamin D – helps absorb Ca in CKD kidney not activating vitamin D so low calcium and High phosphate levels cause even lower calcium levels because calcium binds to phosphate
    o Bone reabsorption associated with the low vitamin D and calcium = osteodystrophy
  • Hyperparathyroidism
    o Parathyroid gland secrete parathyroid hormone when calcium levels are low
    o Parathyroid hormone indirectly influences osteoclast by stimulating the bones to release calcium into the blood = decreased bone health and possible bone pain
161
Q

what does chronic kidney disease do to CV and pulmonary system

A

causes pulmonary edema, HTN, HF, edema

162
Q

why does chronic kidney disease cause pulmonary edema, HTN, HF, edema

A

Symptoms due to fluid overload and metabolic acidosis

163
Q

why does chronic kidney disease cause pericarditis

A

toxin buildup

164
Q

neurologic effect from chronic kidney disease

A

lethargy, Encephalopathy, seizures, coma, Peripheral neuropathy

165
Q

why does chronic kidney disease cause lethargy, Encephalopathy, seizures, coma, Peripheral neuropathy

A
  • Lethargy/dizziness – decrease in red blood cell
  • Encephalopathy, seizures, coma – accumulation of uremic toxins
  • Peripheral neuropathy – uremic toxins also
166
Q

why does chronic kidney disease cause Anemia, epistaxis (nose bleed), bruising

A

because of the reduced erythropoietin secretion and toxins alter platelet function. patient can look pale

167
Q

why does chronic kidney disease cause N/V and anorexia

A

retention of metabolic acids and waste products

168
Q

what type of skin problems can you see on a CKD patient

A

pruritic excoriations, frost, sallow pigmentation, discolored nails

169
Q

pruritic excoriations

A

due to deposits of urea crystals on skin “frost”- this is because of the build up of urea

170
Q

frost

A

uremic frost – urea coming out of skin and causes a little yellow shine

171
Q

sallow pigmentation

A

retention in urochromes which contributes to sallow yellow color

172
Q

CKD and muscles

A

myopathy (muscle weakness) – due to decrease amount of protein

173
Q

what can CKD do to reproductive health

A
  • overall reduced level of sex hormones
  • amenorrhea (absence of menstruation) – reduced level of estrogen
  • impotence- men may have a reduction in testosterone
  • infertility – low sperm count and germinal cell dysplasia
174
Q

why can CKD pt have hypothyroidism

A

Uremia delays the response of thyroid stimulating hormone receptors and Ts levels are often low

175
Q

insulin resistance in chronic kidney pt

A

Related to proinflammatory cytokines and alterations in adipokines (causes high leptin and low adiponectin)

176
Q

dyslipidemia in chronic kidney pt

A

Uremia causes deficiency in lipase

177
Q

what happens to your immune system with CKD

A

Immune system is suppressed due to uremia (high level of urea in blood)

178
Q

how much should an adult pee each day

A

1-2 liters

179
Q

what structure actually produces the urine

A

nephrons

180
Q

what shows up in urine during CKD

A

protein and blood

181
Q

what hormones are produced by the kidney

A

EPO (erythropoietin) and renin

182
Q

what happens with the hormones the kidney produces in CKD

A

EPO is low so pt could be anemic. Glomerulus filtering less water - so body thinks we have low BP so it releases renin to increase BP - even more fluid volume

183
Q

more protein in urine =

A

more endothelial destruction

184
Q

Two factors that Have consistently been recognized to Advanced renal disease

A

proteinuria and Angiotensin II activity

185
Q

why do CKD pt get metabolic acidosis

A

because there is a diminished ability to excrete H+ and generate bicarb which leads to acidosis

186
Q

EKG during hypokalemia

A

long QU interval and prominent U waves

187
Q

EKG during hyperkalemia

A

peaked T waves

188
Q

EKG during hypocalcemia

A

QT prolongation

189
Q

EKG during hypercalcemia

A

shortening of the ST segment

190
Q

steps to late stage of CKD

A
  1. HTN in arteries going to the kidney which causes release of renin which causes more HTN and over time will cause vessel thickening and narrowing which will lead to glomerulosclerosis.
  2. sclerosis causes ischemic injury and nephron loss
  3. nephrons are compensating for other lost nephrons so there is glomerular hyperfiltration that is tolerated during early stages, but not in late
  4. hyperfiltration causes more sclerosis from the pressure
  5. more loss if nephrons
  6. nephrons can not compensate any more and you have a decrease in GFR
191
Q

what causes proteinuria

A

increased capillary permeability which allows protein to pass through and causes loss of negative charge and protein spills into interstitial space

192
Q

what leads to nephron injury and ischemia

A

inflammation, hyperfiltration, and permeability to protein which causes increases pressure in the kidneys and decreased blood flow which leads to ischemia

Nursing school level 2 (15 decks)

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