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NUR 340 > Final Exam: New material > Flashcards

Final Exam: New material Flashcards

1
Q

What is Grey-Turner’s sign

A

Purplish discoloration on the flanks or around the 11th/12th ribs
- indicative of renal injury

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2
Q

which lab values are evaluated to check kidney function

A
  • BUN (not conclusive)
  • creatinine (reflects GFR)
  • GFR (kidney function)
  • osmolality (hydration)
  • anion gap (acid/base balance in blood)
  • hemoglobin/hematocrit (hydration status)
  • albumin (high = dehydration)
  • electrolytes (especially potassium, calcium, phosphorus)
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3
Q

What are the components of a urinalysis

A
  • pH
  • specific gravity/osmolarity
  • glucose
  • protein
  • electrolytes
  • sediment
  • blood
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4
Q

What is dark brown (coca-cola) colored urine indicative of

A

Rhabdomyolysis
color is due to the myoglobin present in the urine

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5
Q

What does it mean if there is protein in the urine

A

Measure of nephron injury/repair

The type of protein depends on the type of kidney disease (low molecular weight protein vs. albumin)

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6
Q

What is GFR

A

Glomerular filtration rate
best measure of kidney function

> 60 = loss of 50% (or more) of normal kidney function

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7
Q

How do we diagnose rhabdomyolysis

A

Blood test will show
- high potassium
- high phosphate
- low calcium
- high uric acid
- high creatinine kinase

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8
Q

What are some causes of rhabdomyolysis

A

Direct muscle tissue damage
metabolic causes
drugs and toxins (statins, antifreeze, SSRIs)

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9
Q

What is rhabdomyolysis

A

Breakdown of muscle tissue usually caused by trauma

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10
Q

What is creatine kinase and what does it tell us

A

A protein found in skeletal muscle
- normal range is > 200
- CK > 1000 = rhabdomyolysis
- CK > 5000 = complications (acute renal failure, DIC, and hyperkalemia)

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11
Q

What is DIC

A

Disseminated intravascular coagulation
Causes abnormal clotting in the vessels

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12
Q

What is the treatment for rhabdomyolysis

A
  • remove cause
  • hyper hydration (4-6 L of fluid in 24 hours)
  • alkalinize urine
  • check CK levels every 4-6 hours
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13
Q

What is creatinine clearance test

A

24 hour urine test
- discard first void
- collect every void in a container for 24 hours
- check urine for creatinine

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14
Q

What symptoms do we see in a patient with a low GFR

A
  • edema
  • decreased output
  • increased BP
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15
Q

What is oliguria

A

reduced urine output
< 400 mL in 24 hours

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16
Q

How much is normal urine output

A

0.5 mL/kg/hour

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17
Q

How is acute kidney injury diagnosed

A

Rise in baseline Cr of at least 0.3 mg/dL in 48 hours, OR 50% higher than baseline in 1 week, OR reduction in urine output > 0.3 mL/kg/hr for 6 hours

Also with a rapid increase of BUN and decrease of GFR

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18
Q

What are the three stages of renal injury

A
  • pre-renal injury
  • intra-renal injury
  • post-renal injury
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19
Q

What is pre-renal injury

A

Due to an issue before the kidney
Decrease in renal blood flow:
- depletion of vascular volume
- impaired perfusion due to HF
- distributive shock
- vasoconstriction of renal vessels (caused by drugs or contrast)
- reversible with treatment

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20
Q

What lab values will we see with pre-renal injury

A
  • Sharp decrease in GFR
  • pre-renal azotemia
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21
Q

What are some things that cause pre-renal injury

A
  • Heart failure (decreased CO)
  • massive bleeding
  • dehydration
  • burns
  • drugs (vasoconstrictors)
  • contrast dye
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22
Q

What is pre-renal azotemia

A
  • BUN/Cr ratio > 20
  • hyaline casts in urine sediment
  • urine specific gravity > 1. 018
  • urine osmolality > 500 mOsm/kg
  • irritants on skin cause itching
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23
Q

What is intra-renal injury

A

Damage to structure within the kidney (glomerular, tubular, or interstitial)
- most commonly tubular (nephron)
- potentially reversible

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24
Q

What are some causes of intra-renal injury

A

Acute tubular necrosis due to:
- ischemia (lack of blood flow)
- nephrotoxic drugs
- tubular obstruction (myoglobin, Hgb, uric acid, myeloma)
- massive infections

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25
Q

What are some nephrotoxic drugs

A
  • chemotherapy agents
  • antibiotics
  • NSAIDs
  • IV contrast dye
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26
Q

What is acute tubular necrosis

A

Destruction of tubular epithelium with acute suppression of renal function

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27
Q

What are the four phases of acute tubular necrosis

A
  • onset (event to injury)
  • oliguric (1-2 weeks)
  • diuretic (1-3 weeks)
  • recovery (up to a year if you get here)
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28
Q

what is the onset phase of ATN

A

Onset of precipitating event until injury to tubule occurs

(taking nephrotoxic drug until damage to tubule occurs)

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29
Q

What are the signs and symptoms of the oliguric phase of ATN

A

Increased BUN/creatinine
- neuro changes: fatigue, confusion
- itching (azotemia)

Hyperkalemia
- EKG changes: tall, peaked T waves, wide QRS, prolonged PR interval

Increased fluid in body
- Edema (risk of pulmonary/cardiac issues)
- hypertension

Metabolic acidosis
- confusion
- Kussmaul breathing

Mild Hyponatremia
- elevated phosphorus
- decreased calcium
- concentrated urine: specific gravity > 1.020

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30
Q

What are the signs and symptoms of the diuretic phase of ATN

A
  • voiding 3-6 L of urine/day
  • GFR improving
  • can filter blood but cannot concentrate urine
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31
Q

What are the signs and symptoms of the recovery phase of ATN

A
  • urine output 1-2 L/day
  • GFR returns to normal
  • BUN/Cr return to normal
  • electrolytes return to normal
    (some patients never make it to recovery)
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32
Q

What is pre-renal azotemia

A
  • BUN/Cr ratio > 20
  • hyaline casts in urine sediment
  • urine specific gravity > 1. 018
  • urine osmolality > 500 mOsm/kg
  • irritants on skin cause itching
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32
Q

What is intrarenal renal failure

A

Renal failure in the tubules of the nephron due to ischemia, toxins from drugs, or toxins from massive infection

Usually caused by drugs: chemo, antibiotics, NSAIDs, or IV contrast dye

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33
Q

What is post renal failure

A

obstruction of urine outflow from the kidneys, to the bladder, and out of the body
- renal calculi in the ureter
- neurogenic bladder or tumors in the bladder
- benign prostatic hyperplasia blocking urine flow in the urethra

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34
Q

What is the most common clinical manifestation of acute renal failure

A

oliguria (abnormally small amounts of urine)

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35
Q

What are the major electrolyte imbalances that we see with acute renal failure

A

Hyperkalemia
Hypocalcemia
Hyperphosphatemia
Hyponatremia

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36
Q

How do we assess for hyperkalemia

A
  • Peaked T waves
  • widened QRS interval
  • can lead to V tach or V fib
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37
Q

How do we treat hyperkalemia

A

Immediately administer calcium, insulin, glucose, and albuterol along with kayexalate or lokalma

  • calcium: stabilizes resting membrane potential to prevent arrhythmias
  • insulin: forces potassium into the cells to lower serum K levels
  • glucose: to prevent hypoglycemia from insulin
  • albuterol: shifts potassium into intracellular space
  • kayexalate: binds K and brings it out in stool
  • lokalma: like kayexalate but doesn’t cause diarrhea
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38
Q

How do we treat hypocalcemia

A

calcium replacement and vitamin D

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39
Q

How do we treat hyperphosphatemia

A

phosphorus binding drugs:
- aluminum
- calcium salts
- Renagel
- Fosrenol

40
Q

What are the major complications of acute renal failure

A

Hyperkalemia
Metabolic acidosis
Anemia
Prolonged bleeding time
Infections
cardiac complications
Malnutrition

41
Q

What is chronic kidney disease

A

The continual and irreversible reduction in nephron number

42
Q

What are some things that can cause CKD

A

Diabetes
Hypertension
Glomerulonephritis
Polycystic disease

43
Q

What is hemodialysis

A

patient with Kidney disease do this three times a week in order to filter toxins out of their blood since their kidneys cant.

a Quinton catheter is inserted into a vein (Usually subclavian but can also use femoral) or a fistula or AV graft (long term use)

44
Q

What is CRRT

A

Continuous renal replacement therapy
- Hemodialysis but continuous

45
Q

What is peritoneal dialysis

A

For patients with CKD; long term dialysis

a catheter is placed in the peritoneum and then is routinely drained and filled with new fluid

Catheter care is very important! (peritonitis)

46
Q

What are some major complications of dialysis

A
  • Hyperkalemia
  • Pericarditis
  • Pericardial effusion
  • Pericardial Tamponade
  • Hypertension
  • Anemia
  • Bone disease and metastatic calcifications
  • ACCESS
  • peritonitis (PD)
47
Q

Wat is uremic frost

A

Yellow crystals on the skin from urea in sweat
usually occurs in BUN > 200

48
Q

What is normal A1C in lab values

A

4-7%

49
Q

What are the actions of insulin

A
  • promote cellular glucose uptake
  • promote glucose storage into glycogen
  • prevents fat and glycogen breakdown
  • inhibits gluconeogenesis
  • increases protein synthesis
50
Q

What are the characteristics of type I diabetes

A
  • Always insulin dependent
  • caused by pancreatic beta-cell destruction
  • fatty acids are converted to ketones in liver
51
Q

WHat are the characteristics of type II diabetes

A
  • caused by genetics, drugs, or toxins
  • peripheral insulin resistance
  • increased glucose production in liver
  • upper body obesity
52
Q

What are the criteria for metabolic syndrome

A
  • abdominal obesity
  • triglycerides > 150
  • HDL < 50
  • BP > 130/85
  • fasting glucose > 110
53
Q

What are some symptoms of diabetes

A
  • polydipsia
  • polyuria
  • polyphagia
  • thirst
  • hunger
  • weight loss (Type I)
  • blurred vision, fatigue, paresthesia, and skin infection (Type II)
54
Q

What are some medical management methods for diabetes

A
  • diet
  • exercise
  • insulin (injections, inhalations, and pumps)
  • oral medications
55
Q

What are some oral medications for diabetes

A

Sulfonylureas: beta cell stimulant
Biguanides: prevents glucose production (metformin)
Alpha-glucosidase inhibitors: stop carb absorption in small intestine
Thiazolidinediones: insulin sensitizers

56
Q

What are some common insulin medications

A

aspart (Novolog) - ultra-short acting

glulisine (Apidra) - ultra short acting

lispro (Humalog) - ultra short acting

Human regular (Humulin R or Novolin R) - short acting

Human NPH (Humulin N or Novolin N) - intermediate

Detemir (Levemir) - long acting

glargine (Lantus) - long acting

57
Q

What is diabetic neuropathy

A

somatic neuropathy- loss of sensation of pain, vibration, and temperature and increased sensation to light touch (feels like burning)

Autonomic neuropathy - loss of function in autonomic processes such as vasomotor, cardiac, GI (gastroparesis), neurogenic bladder, and sexual dysfunction

58
Q

What are the signs and symptoms of hypoglycemia

A
  • hunger
  • anxiety
  • tachycardia
  • sweating
  • cool, clammy skin
  • altered mental status
  • seizures
  • coma
59
Q

What are some treatments for hypoglycemia

A

1/2 cup of juice followed by starch and protein
- cheese/crackers, milk/crackers, ham sandwich

1 amp D50 IV push (100 calories)
- half life only 30 minutes

60
Q

What is diabetic ketoacidosis

A

Seen in type 1
caused by
- physical stressors (surgery, infection, trauma)
- low insulin (diet/exercise changes, faulty insulin pump)
- pregnancy
- growth spurts
- emotional stress
- drugs (steroids, epinephrine/norepinephrine)

61
Q

How is DKA diagnosed

A
  • Glucose > 300
  • HCO3 < 15
  • pH < 7.3 (metabolic acidosis with respiratory - alkalosis to compensate)
  • rising anion gap
  • urine ketones
  • sudden onset
62
Q

What are the signs and symptoms of DKA

A
  • polyuria
  • polydipsia
  • polyphagia
  • severe fatigue
  • fruity breath
  • kussmaul breathing
  • N/V
  • hypovolemia (hypotension, tachycardia)
63
Q

What are the treatment methods for DKA

A
  • correct insulin problem (fix pump)
  • give fluids
  • correct acidosis but DO NOT give HCO3 unless in cardiac arrest
  • do not treat hyperkalemia because insulin will drop serum K
  • careful, low doses of insulin IV (extreme acidosis can cause insulin resistance)
  • add glucose to insulin IV when sugar < 200-250 to avoid hypoglycemia
  • monitor anion gap
64
Q

What is hyperglycemic hyperosmolar state

A

Seen in type II diabetes
caused by
- insufficient insulin
- infection

65
Q

How do we diagnose HHS

A
  • Hyperglycemia > 600
  • hyperosmolarity > 320 mmols/kg
  • dehydration
  • absence of acidosis
  • ketones absent or mild
  • gradual onset
66
Q

what are the signs and symptoms of HHS

A
  • glucose > 600
  • polyuria
  • polydipsia
  • dehydration (dry mucous membranes, tented skin turgor)
  • fever
  • fatigue
  • mental status changes (confusion, seizure)
  • coma
67
Q

What is the treatment method for HHS

A
  • Meticulous rehydration
  • Replacement of K
  • monitor fluid status and neuro status
  • treat underlying cause
68
Q
A
69
Q

What is diabetes insipidus

A

Insufficiency of antidiuretic hormone (ADH)
- ADH makes tubules reuptake water
- large amounts of water are lost
- leads to dehydration, hypernatremia, and hypovolemia/hypotension

70
Q

What are the three types of diabetes insipidus

A

Central - birth defect/unknown cause
nephrogenic - no response to ADH from kidney
psychogenic - rare; compulsive water drinking

71
Q

How do we diagnose diabetes insipidus

A
  • Urine output > 300 mL/hr
  • Low urine specific gravity
  • High serum osmolality
  • Hypernatremia
  • Check ADH levels (either there isn’t enough or the kidneys aren’t responding to it)
72
Q

How do we treat diabetes insipidus

A
  • Treat cause
  • Hourly urine output (match with IV intake)
  • Vasopressin (for central DI)
  • Desmopressin (DDAVP) for less severe cases
  • Thiazide diuretics (nephrogenic DI)
73
Q

Why give a diuretic for diabetes insipidus

A

Thiazide diuretics help shift fluid back where it needs to be rather than having the patient pee it out

74
Q

What is syndrome of inappropriate antidiuretic hormone (SIADH)

A

Opposite of diabetes insipidus
- too much ADH
- kidney reabsorb too much water
- hyponatremia

75
Q

What causes SIADH

A
  • Head trauma (damage to hypothalamus)
  • small cell carcinoma
  • stress
  • medications (thiazides, chemo)
76
Q

How do we diagnose SIADH

A

Sodium < 120
serum osmolality < 250
concentrated urine (high specific gravity)
low urine output

77
Q

What are the signs and symptoms of SIADH

A
  • lethargy
  • confusion
  • anorexia
  • seizure
  • coma
  • death
78
Q

How do we treat SIADH

A
  • Fluid restriction < 500 mL
  • hypertonic NaCl infusion (3-5%)
  • stop drugs that can cause SIADH
  • monitor hydration status
  • seizure precautions
79
Q

Compare SIADH to DI:
- urine output
- ADH levels
- sodium levels
- hydration status
- movement of fluid

A
80
Q

What are the signs and symptoms of high cortisol levels

A
  • extreme fatigue
  • weight loss
  • decreased appetite
  • dehydration
  • darkening of skin
  • low blood pressure
  • fainting
  • salt craving
  • low blood sugar
81
Q

What is Cushing’s syndrome

A

Hypersecretion of cortisol
caused by :
- pituitary creates too much adrenocorticotropic hormone (ACTH)
- glucocorticoid therapy

82
Q

what are the signs and symptoms of Cushing’s Syndrome

A
  • fragile skin
  • truncal obesity
  • round face
  • sexual dysfunction (amenorrhea/ED)
  • bruising
  • hypertension
  • purple striae on abdomen and extremities
  • hyperglycemia
  • excessive body hair in women
  • hypokalemia
  • buffalo hump
  • depression
83
Q

What is Addison’s disease

A

Hyposecretion of cortisol and aldosterone
caused by:
- autoimmune disease
- tuberculosis/infections
- cancer
- trauma

84
Q

What are the signs and symptoms of Addison’s disease

A
  • hypoglycemia
  • hyponatremia
  • salt cravings
  • fatigue
  • muscle weakness
  • hyperkalemia
  • hypercalcemia
  • irregular menstruation/ED
  • hypotension
  • darkening of skin
  • diarrhea
  • nausea
  • depression
85
Q

What are the 5 S’s of Addison crisis

A

S - Sudden pain (in stomach, back, and legs)
S - Syncope
S - Shock
S - Super low BP
S - Severe vomiting, diarrhea, headache

86
Q

Signs and symptoms of hyperthyroidism

A
  • weight loss
  • heat intolerance
  • tachycardia
  • hypertension
  • diarrhea
  • smooth skin
  • soft hair
  • dysrhythmias: a-fib
  • personality changes: irritability, insomnia
  • irregular menstruation
87
Q

What is thyroid storm

A

life threatening condition that’s caused by uncontrolled hyperthyroidism. Same symptoms except worse plus fever

TSH very low
T3 and T4 very high
hypocalcemia

88
Q

How do we treat hyperthyroidism

A

radioactive iodine
thyroidectomy

89
Q

What do we need to teach patients who are taking radioactive iodine

A

avoid iodine rich food: sea food, dairy, eggs
no aspirin: increases thyroid hormone
signs and symptoms of hypothyroidism

90
Q

What is Grave’s Disease

A

autoimmune hyperthyroidism
S/S: protruding eyes, goiter, thin body, jittery

91
Q

What is myxedema coma

A

severe hypothyroidism with hypothermia and coma; usually believed that pt is just depressed
- confused
- hypothermic
- waxy buildup on skin

92
Q

What is Pheochromocytoma

A

Tumor of the adrenal medulla
Causes: 5 H’s
H - hypertension
H - headache
H - hyperglycemia
H - hyper metabolism
H - hyperhidrosis (excessive sweating)

93
Q

What are the 4 stages of shock

A

initial: S/S hard to pinpoint

compensatory: body tries to reverse condition

progressive: multiorgan symptoms (compensation failed) MAP < 60

refractory: unmanageable; organs begin to fail

94
Q

What is the SIRS criteria

A

Systemic inflammatory response system: assessment for shock (usually sepstic)

Temp > 38 or < 36
HR > 90
RR > 20
CO2 < 32

95
Q

What do we do for MODS (multiorgan dysfunction syndrome)

A
  • fluid resuscitation
  • hemodynamic support
  • treat infection
  • prevent further infection
  • maintain tissue oxygenation
  • nutritional support
  • comfort
  • support individual organ function
96
Q

What do we do for septic shock

A
  • vasopressors
  • fluids
  • blood cultures
  • antibiotics
  • emotional support
  • monitor for complications
97
Q

What are the signs and symptoms of hypovolemic shock

A

low bp
tachycardia
low urine output
cool clammy skin
mental status changes
tachypnea
swaeting

NUR 340 (10 decks)

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