Management of Other Body Systems Flashcards

1
Q

what is diabetes mellitus?

A

chronic metabolic disorder characterized by elevated blood glucose levels (hyperglycemia) caused by defects in insulin secretion (from the pancreas), insulin action, or both

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2
Q

glucose can’t be utilized w/o ____

A

insulin

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3
Q

what is type 1 DM?

A

autoimmune destruction of the pancreas beta cells resulting in absolute insulin deficiency (body doesn’t produce insulin)

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4
Q

what are the key features of type 1 DM?

A

sudden onset, often in childhood/adolescence

presence of autoantibodies (ie islet cells antibodies)

dependence of exogenous insulin for survival

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5
Q

what are the complications of type 1 DM?

A

ketoacidosis, microvascular, and macrovascular damage

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6
Q

what is type 2 DM?

A

progressive insulin resistance and relative insulin deficiency

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7
Q

which type of DM has genetic predisposition and lifestyle contributing factors?

A

type 2

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8
Q

which type of DM has a gradual onset, typically in adults?

A

type 2

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9
Q

what are the key factors of type 2 DM?

A

insulin resistance in target tissues (muscle, liver, adipose)

impaired insulin secretion by pancreatic beta cells

often associated with obesity and metabolic syndrome

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10
Q

what are the complications of type 2 DM?

A

CV disease, neuopathy, nephropathy, retinopathy

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11
Q

what is the fasting plasma glucose levels with type 2 DM?

A

greater than or equal to 126 mg/dL

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12
Q

what is the 2 hour plasma glucose with type 2 DM?

A

greater than or equal to 200 mg/dL during OGTT

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13
Q

what is the HbA1c with type 2 DM?

A

greater than or equal to 6.5%

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14
Q

what does HbA1c measure?

A

blood sugar levels over the last 3 months

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15
Q

what happens when glucose isn’t being taken up?

A

w/o insulin, glucose is unable to be processed by the body

liver produces more glucose to feed the body, but w/o insulin, the glucose accumulates in the bloodstream

the body needs an alternative energy source so it breaks down fat, the fat breakdown produces ketones which buildup in the bloodstream

ketones and glucose are transferred into the urine and the kidneys use water to clear the blood from excess glucose and ketones

while the body attempts to get rid of the ketones and glucose, a lot of water is lost which can lead to dehydration and may worsen ketoacidosis

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16
Q

what is diabetic ketoacidosis?

A

when there is an insulin deficiency, the body breaks down fats bc it can’t use glucose for energy, which causes a buildup of ketones in the blood

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17
Q

what is the primary trigger for diabetic ketoacidosis?

A

insulin deficiency

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18
Q

what are the characteristics of diabetic ketoacidosis?

A

hyperglycemia

ketosis

metabolic acidosis

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19
Q

what is hyperglycemia?

A

high blood sugar (>250 mg/dL blood glucose) leading to osmotic diuresis and dehydration

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20
Q

what is ketosis?

A

accumulation of ketones caused by breakdown of fatty acid causing a metabolic acidosis

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21
Q

what are the ketone bodies produced?

A

acetoacetate

beta hydroxybutyrate

acetone

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22
Q

what may be the initial presentation in about 25-40% of type 1 diabetics?

A

ketoacidosis

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23
Q

what may occur in at least 34% of those with type 1 DM

A

ketoacidosis

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24
Q

what is the leading cause of morbidity/mortality in DM?

A

ketoacidosis

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25
Q

what are the clinical manifestations of ketoacidosis?

A

polyuria

polydipsia

polyphagia

altered mental status

nausea, vomiting, abdominal pain

rapid breathing

fruity breath odor

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26
Q

what is polyuria?

A

frequent urination

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27
Q

what is polydipsia?

A

excessive thirst

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28
Q

what is polyphagia?

A

excessive hunger

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29
Q

why does rapid breathing occur with ketoacidosis?

A

as a compensation for metabolic acidosis

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30
Q

why is there fruity breath with ketoacidosis?

A

acetone production

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31
Q

t/f: organs don’t work as well with high ketones

A

true

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32
Q

what are the symptoms of ketoacidosis?

A

high BG

foul odor breath

stomach ache with or without vomiting

severe cases can have trouble breathing

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33
Q

what are the causes of high BG in ketoacidosis?

A

forgetting to take insulin

using expired insulin or insulin not properly stored

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34
Q

what is the treatment of high BG in ketoacidosis?

A

check ketones if the BG is >300 mg/dL or when sick

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35
Q

what is the cause of foul odor breath in ketoacidosis?

A

illness

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36
Q

what is the treatment of foul odor breath in ketacidosis?

A

call the doctor if ketones are present

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37
Q

what is the cause of nausea with or without vomiting in ketoacidosis?

A

wrong dose insulin

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38
Q

what is the treatment for nausea in ketoacidosis?

A

drink extra water or sugar free liquids to stay hydrated

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39
Q

what is the cause of trouble breathing in severe cases of ketoacidosis?

A

insulin pump NOT working

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40
Q

what is the treatment for trouble breathing in severe cases of ketoacidosis?

A

DON’T exercise until ketones are no longer present

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41
Q

why is reduced EF with HF an issue?

A

bc not as much blood is being pumped out leading to poor endurance, elevated HR, OH, and tiredness

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42
Q

what conditions may result from ketoacidosis that need medical management?

A

severe ischemic cardiomyopathy with acute HF with reduced EF

hypoxic respiratory failure

NSTEMI/acute coronary syndrome

hypokalemia/hypomagnesemia

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43
Q

what other organ systems should we consider with diabetic pts?

A

endocrine

cardiac

pulmonary

renal

liver

hematology

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44
Q

what systems are included in the PT systems review?

A

MSK

CVP

integ

neuro

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45
Q

what are the exercise considerations with DM?

A

insuline injection timing, place, and type

HR response

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46
Q

t/f: we want pts with DM to have stable glucose levels b4 working with them

A

true

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47
Q

b4 working with a pt with DM, where do we want there BG levels?

A

80-100

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48
Q

if a pt has low BG, what should we do?

A

give them juice or a sugar tablet

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49
Q

after a pt is extubated, what should we do?

A

a cough assessment and breathing exercises

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50
Q

during day 1 in acute care, what are we doing?

A

early mobilization

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51
Q

during day 3 in acute care, what are we doing?

A

EOB

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52
Q

during day 6 in acute care, what are we doing?

A

independent ambulation

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53
Q

during day 8 in acute care, what are we doing?

A

D/C?

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54
Q

what is hypovolemic shock a result of?

A

fluid loss

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55
Q

what is caridogenic shock a result of?

A

ineffective heart pump

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56
Q

what is septic shock a result of?

A

infection

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57
Q

what does any type of shock lead to?

A

multisystem organ failure

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58
Q

what is the renal function?

A

to filter the blood and tightly control electrolytes

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59
Q

what are the 4 major functions of the kidneys?

A

filtration of the blood and excretion to remove wastes

regulation of electrolyte balance for tight control of Na, K, Cl, and P

regulation of pH or acid/base balance

regulation of blood volume and BP

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60
Q

what is the renin-angiotensin-aldosterone mechanism?

A

decreased Bp stimulates special cells in the kidneys that release renin in the blood

renin cleaves off part of the plasma proteins, angiotensin, that triggers an enzyme cascaderesulting in conversion to angiotensin 2 (a potent stimulator of aldosterone release) leading to aldosterone release

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61
Q

what turns angiotensin 1 to angiotensin 2?

A

ACE

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62
Q

what is glomerular filtration rate (GFR)?

A

the volume of nitrate formed by both the kidneys per minute

63
Q

the heart pumps about how many liters of blood per minute under resting conditions?

A

5L

64
Q

the heart pumps about 5L of blood per minute under resting conditions, which is about ___% of CO

A

25

65
Q

what % of blood pumped per minute enters the kidneys to be filtered?

A

20%

66
Q

how many liters of blood are pumped per day in males?

A

180 L

67
Q

how many liters of blood are pumped per day in females?

A

150 L

68
Q

what % of the filtrate of blood is returned to circulation by reabsorption?

A

99%

69
Q

about how many liters of urine are produced per day?

A

1-2 L

70
Q

what are the characteristics of pre-renal failure?

A

drop in CO

reduced GFR

CMP changes

decreased urine output

71
Q

t/f: there is s drop in blood volume due to GI loss leading to a drop in MAP in pre-renal failure

A

true

72
Q

t/f: there is reduced renal blood flow and subsequent perfusion of fewer nephrons in pre-renal failure

A

true

73
Q

what are the CMP changes in pre-renal failure?

A

reabsorption of Na to limited fluid loss in an attempt to increase blood volume

altered electrolyte balance: elevated K, BUN, and creatinine

74
Q

what are the characteristics of renal failure?

A

prolonged drop in CO

decreased urine output

CMP changes

75
Q

does pre-renal failure or renal failure have a drop in CO that is unresponsive to a fluid bolus (not peeing out what they are taking in) and acute tubular necrosis?

A

renal failure

76
Q

decreased urine output in renal failure is due to what?

A

proximal and distal convoluted tubules not reabsorbing Na bc water follows Na

77
Q

what are the CMP changes in renal failure?

A

15:1 ratio of BUN:Cr

altered electrolyte balance: low K, high BUN, high Cr

78
Q

what are the different types of renal replacement therapy (RRT)?

A

IHD (intermittent)

CRRT (continuous)

PIRRT (peritoneal)

79
Q

t/f: CRRT provides more gradual fluid removal and solute clearance over prolonged treatment times compared to intermittent

A

true

80
Q

what pts often use CRRT?

A

hemodynamically unstable pts

81
Q

where are the common access points for RRT?

A

subclavian

internal jugular

femoral

82
Q

what is the progression of liver failure?

A

healthy liver–>fatty liver–>liver fibrosis–>liver cirrhosis

83
Q

what is the most common form of liver failure we will see?

A

fatty liver disease (alcoholic of non-alcoholic)

84
Q

what are the various causes of liver disease?

A

fatty liver diseases

viral (hep B, C, D)

autimmune

chronic biliary disease

cardiovascular

storage diseases

other rare causes

85
Q

what is the score used to classify liver one year survival rates?

A

Child-Pugh score

86
Q

what is the score used to determine the severity of liver disease for transplantation?

A

MELD (model for end-stage liver disease)

87
Q

what is the MELD score?

A

a combo of INR, creatinine, bilirubin, and sodium to create a score of 0-40 (higher score=higher severity) to determine liver disease severity for transplant

88
Q

pts with a MELD score >___ will have their MELD re-calculated weekly

A

25

89
Q

if sarcopenia is accounted for in MELD, how many points are added?

A

10

90
Q

what causes jaundice?

A

increased bilirubin

91
Q

if someone has liver necrosis, what are two key signs to look for?

A

light color stool

dark urine

92
Q

t/f: alcoholic liver disease is a spectrum of disease which includes fatty liver w/ or w/o hepatitis, alcoholic hepatitis to cirrhosis

A

true

93
Q

pt with severe alcohol use disorder mostly develop what disease?

A

chronic liver disease

94
Q

what is the most frequent cause of CLD (chronic liver disease)?

A

severe alcohol use disorder

95
Q

what is at risk drinking for men?

A

> 14 drinks/week
OR
4 drinks/occasion

96
Q

what is at risk drinking for women and those over 65?

A

> 7 drinks/week
OR
3 drinks/occasion

97
Q

more than ___ drinks/week in men is severe drinking from a liver toxicity standpoint

A

21

98
Q

more than ___ drinks/week in women is severe drinking from a liver toxicity standpoint

A

14

99
Q

what % of pts w/liver cirrhosis have hepatopulmonary syndrome?

A

5-32%

100
Q

what is hepatopulmonary syndrome?

A

a combo of liver dysfxn or portal HTN, intrapulmonary vascular dilation, and abnormal oxygenation

101
Q

what are the s/s of hepatopulmonary syndrome?

A

SOB (esp with sitting, standing, or exertion)

digital clubbing

spider angioma

cyanosis

102
Q

what is spider angioma?

A

like varicose veins but much smaller and seen throughout the body

103
Q

t/f: spider angioma is NOT a good sign

A

true

104
Q

t/f: SpO2 can drop very quickly with hepatopulmonary syndrome, but we still have to mobilize them

A

true

105
Q

the initial screening for hepatopulmonary syndrome involved what VS?

A

pulse ox to evaluate PaO2

106
Q

O2 sat <____% indicates PaO2<70mmHg and is considered a (+) screen for hepatopulmonary syndrome

A

96

107
Q

how is hepatopulmonary syndrome treated?

A

transplant

108
Q

what are the implications of hepatopulmonary syndrome?

A

pace activities or maybe not able to treat

109
Q

what is portal HTN?

A

when pressure of the blood entering the liver (via portal veins) is greater than the pressure of the blood in the inferior vena cava blood gets backed up and causes engorged veins (esp at the stomach and esophagus) and can lead to varicies and gastroesophageal bleeding

110
Q

how is portal HTN treated?

A

beta blockers

transjugular intrahepatic portosystemic shunt (TIPS)

111
Q

what is TIPS?

A

it’s a shunt that creates a bypass bw the portal vein and the hepatic vein

112
Q

what are the implications of portal HTN?

A

make sure the pt is breathing (look for Valsalva)

highest pressures occur at night, after eating, and in response to coughing, sneezing, and exercise

GI bleeds

113
Q

when a pt has portal HTN, what should we teach them?

A

how to modify and reduce pressure with anything that increases intraabdominal pressure (ie, coughing, straining at stool, improper lifting)

114
Q

what should we do with pts with portal HTN and GI bleeds?

A

monitor hemodynamics

weigh the risks vs benefits of mobilization with a recent bleed

s/s monitoring

115
Q

what are the s/s of a GI bleed?

A

anemia

fatigue

SOB

dark stool is above the stomach (upper GI bleed)

116
Q

what is hepatic encephalopaty (HE)?

A

a significant complication from liver disease caused by liver insufficiency and/or portal systemic shunting that results in elevated ammonia and systematic inflammation that causes significant neurocognitive changes

117
Q

a pt with HE may have elevated levels of what?

A

ammonia (a neurotoxin)

118
Q

t/f: HE causes significant neurocognitive changes

A

true

119
Q

what are the symptoms of HE?

A

change in personality

agitation

lethargy

inappropriate behavior

confusion

coma

120
Q

what is the incidence of HE?

A

30-40% of pts with liver disease develop HE

121
Q

how is HE treated?

A

lactulose to release ammonia production and absorption

anti-microbials

122
Q

what grade HE is a pt dependent but good for d/c?

A

grade 1

123
Q

what grade HE is the goal to protect the pt from harm?

A

grade 2

124
Q

what grade HE is the priority positioning?

A

grade 4

125
Q

what is sarcopenia?

A

a condition of low muscle mass as evidenced by reduced muscles cross sectional area cause by an imbalance bw protein synthesis and breakdown

126
Q

what may sarcopenia be caused by?

A

dietary intake

portal HTN complications

pro-inflammatory cytokines

hyperammonemia

limited physical activity

127
Q

what is the incidence of sarcopenia?

A

as high as 30-70% of pts w/liver failure

128
Q

how is sarcopenia treated?

A

nutrition (specifically protein and BCAA)

physical exercise

meds (vit D in geriatrics but not researched)

129
Q

what are the implications of sarcopenia?

A

there is a higher risk for complications, longer LOS in hospital, poorer clinical outcomes post-transplant, and mortality

anticipate fxnal mobility deficits

130
Q

what % of pts with liver cirrhosis have ascites?

A

5-10%

131
Q

what is the most common complication of cirrhosis resulting from portal HTN and liver insufficiency?

A

ascites

132
Q

what is the theory behind why ascites occurs?

A

reorganization of hemodynamics (inc hydrostatic pressure)–>inc vasodilation–> sodium and water retention

133
Q

how is ascites treated?

A

diuretics

regular out of bed activities

large volume paracentesis (needle draws out fluid)

sodium restriction

albumin infusion

134
Q

when would we use large volume paracentesis removal with ascites?

A

when there is so much fluid the pt can’t breathe

135
Q

what are the implications of ascites?

A

physical exam

monitor body mechanics

assess for edema

balance

positioning considerations for respiratory function

136
Q

what position should be avoided with ascites?

A

supine bc it makes it difficult for them to breathe

137
Q

what is the reference range for bilirubin?

A

0.2-1.3 mg/dL

138
Q

what is bilirubin?

A

an orange-yellow colored waste formed in the liver from the breakdown of hemoglobin that is normally excreted by bile

139
Q

if bilirubin is high, what does this mean?

A

the liver isn’t flushing waste efficiently

140
Q

what physical exam findings would be present with high bilirubin?

A

jaundice

yellow sclera

141
Q

what is the reference range for ammonia?

A

15-60 mcg/dL

142
Q

what is ammonia?

A

a nitrogen waste product normally excreted via urine

143
Q

if ammonia is high, this could mean that kidney/liver fxn is correlated to what?

A

HE

144
Q

what is the reference range for creatinine?

A

0.38-1.02 mg/dL

145
Q

what is creatinine?

A

a waste products produced by muscle breakdown of creatine

normally flushed from the body via the kidneys which filter almost all of it from the blood to urine

146
Q

if creatinine is high, what could this mean?

A

kidney problems

147
Q

t/f: if a pt has high creatinine, they may have a reduced ability to clear medications

A

true

148
Q

what is the reference range for albumin?

A

3.5-5.2 g/dL

149
Q

what is albumin?

A

a liver protein that maintains osmotic pressure of the blood compartment

provides tissue nourishment

transports hormones, vitamins, drugs, and other substances throughout the body

150
Q

what is the reference range for INR?

A

0.8-1.3

151
Q

how is the INR calculated?

A

fromt he PTT (# of sec it takes for a sample of blood to clot when a reagent is added)

152
Q

if INR is high, what is the risk?

A

bleeding

fall risk

exercise intolerance

153
Q

what is included in observation for liver disease?

A

abdominal girth

muscle wasting

integ color integrity, edema

154
Q

what is included in the physical exam for liver disease?

A

abdominal palpation for hepato/splenomegaly

posture

strength testing

balance

endurance