Complex Critical Illness (F&E, Liver) Flashcards
1
Q
ADH
A
- stimulates water reabsorption by opening little channels in the
collecting duct - water moves through channels from area of lower [ ] (collecting duct) to area of higher [ ]
(blood)
2
Q
ADH release is triggered by:
A
- osmotic sensors in the hypothalamus which react to the concentration of solutes in your blood.
- baroreceptors in the left atrium, carotid artery and aortic arch react to decreased arterial pressure
- baroreceptors in the right atrium and vena cava’s react to less
volume returning to heart - RAAS
3
Q
aldosterone
A
- released by adrenal cortex
- triggers reabsorption of Na+ from the nephron collecting duct back
into bloodstream - water is also reabsorbed
- both fluid and solutes are moving in proportion to each other
4
Q
aldosterone release is triggered by
A
- stress response of the hypothalamus (considered a stress hormone along with cortisol)
- RAAS
5
Q
ANP and BNP
A
- release in response to myocardial stretch
- cause vasodilation, loss of sodium and water in nephron, and inhibit SNS and RAAS
- results in inc urine o/p, dec preload d/t dec blood volume, does not impact osmolality
- both fluid and solutes are moving out of the blood in proportion to each other
6
Q
ANP and BNP release is triggered by:
A
ANP - secreted by atrium, triggered by hyperNA and myocardial stretch
BNP - secreted by ventricles, triggered by myocardial stretch
7
Q
hematocrit
A
- ratio of RBC to total volume of blood
- indicator of concentration
- follow as a trend
low Hct = more dilute
high Hct = more concentrated
8
Q
blood is expressed as a?
A
concentration
9
Q
isotonic
A
same osmolality between
plasma and cells
10
Q
hypotonic
A
lower osmolality in plasma compared to cells
11
Q
hypertonic
A
higher osmolality in
plasma compared to cells
12
Q
tonicity
A
- ability of a solution to make water move in and out of cells
- solutions are described in relation to their osmolality relative to
plasma
13
Q
hypertonic disorders
A
when H2O is lost but solutes in the blood
remain the same, the intravascular fluid volume becomes more concentrated
14
Q
hypotonic disorders
A
when H2O is in excess, but solutes remain the
same, the intravascular fluid volume becomes less concentrated
15
Q
what is the major ion of the ECF?
A
Na
16
Q
what does a low sodium level reflect/not reflect?
A
does not reflect an overall loss of sodium ion –
it reflects less sodium ions/per unit of volume
17
Q
what does excess H2O cause? what is it caused by? tx?
A
- hypotonic disorder, caused by SIADH or admin of too much water
- hyponatremic hypervolemia
- tx = diuretics or limit H2O
18
Q
SIADH - patho, s/s, tx
A
patho
- excess ADH secretion, fluid retained by kidneys, decreased u/o
s/s
- dilute blood, decreased serum Na and osmolality
- concentrated urine, increased urine Na, osmol, specific gravity
tx
- restrict fluid, replace Na w/ 3%, monitor for seizures/inc ICP/dec LOC
19
Q
deficit of H20: what does it cause? caused by? tx?
A
- hypertonic disorders, caused by severe diarrhea or vomiting or DI
- hypernatremic hypovolemia
- tx: infuse D5W or add H20 flush
20
Q
what does a high sodium level reflect/not reflect?
A
does not reflect an overall increase of sodium ion – it reflects more sodium ions/per unit of volume
21
Q
DI: patho, s/s, tx
A
patho
- decreased ADH is produced, kidneys unable to retain fluid, increased u/o
s/s
- concentrated blood: inc serum Na and osmolal
- dilute urine: decreased urine Na, osmol, sp grav
tx
- ?give H20
- give ADH
- monitor urine o/p, specific gravity
22
Q
potassium functions
A
- nerve impulse conduction
- myocardial, smooth, and skeletal muscle contraction
- acid base balance
23
Q
potassium regulation
A
- passively diffuses out of cell, actively transported back in Na/K pump
- kidney regulates balance of Na and K
24
Q
in acidosis, what enters the cell and what leaves the cell?
A
H+ enters the cell and ICF, K and Mg leave the cell
25
movement of glucose into the cells also drives ___ into cells
K+
26
hypokalemia causes
alkalosis
diuretics
aldosterone release
GI losses
27
hypokalemia manifestations
flattened T waves
dysrhythmias
skeletal muscle weakness
28
hyperkalemia causes
kidney failure
acidosis
cell injury/lysis
29
hyperkalemia manifestations
peaked T waves
dysrhythmias
skeletal muscle weakness
n/v
30
hypokalemia tx
tx underlying cause, stop meds (diuretics), replace lost K
31
hyperkalemia tx
- tx underlying cause
- remove excess K
- shift with D50 and insulin
32
sodium functions
- maintain fluid balance in the body
- Extracellular osmolality
- Nerve impulse – Na/K pump
- Helps regulate acid-base
33
sodium regulation
- regulated primarily by Kidneys – secrete/ reabsorb. Controlled by
osmoreceptors
- Aldosterone vs. ANP (inverse rel'n)
- ADH
34
hyponatremia causes
- Dilutional – too much free water, SIADH, oliguric renal failure, hyperglycemia (retains H20)
- Low intake – rare
- Loss of Na – diuretics, sweating
35
hyponatremia manifestations
- neuro changes
- muscle weakness
36
hypernatremia causes
- Water deficit – dehydration, DI
- Loss of hypotonic solutions
- Excess intake (rare),
hyperaldosteronism (Cushings Disease)
37
hypernatremia manifestations
- Neurological – confusion, twitching, seizures, coma (cells shrivelled + changes to action potentials)
- Thirst
- High serum osmo
38
hyponatremia management
- limit free water
- ?diurese excess water
- ? 3% NS - severe cases
39
hypernatremia management
- free water (IV or OG)
- limit Na (mix meds in D5)
- tx underlying cause
40
chloride functions
- Maintains fluid osmolality with Na
- Combines to form HCL
- Increased action potential for neurons- making it harder for nerve impulses to fire
41
chloride regulation
- Kidneys – excreted or reabsorbed similarly to Na+
- Acid-base balance
42
hypochloremia causes
- Hyponatremia
- Alkalosis
- Loss of HCL
- Diuretics
43
hypochloremia manifestations
- Similar to hypoNa+ or alkalosis
- CNS – overexcitability, cramps, twitching
- CVS - dysrhythmias
44
hyperchloremia causes
- hypernatremia
- acidosis
45
hyperchloremia manifestations
- Similar to acidosis
- CNS – lethargy, coma (severe)
- CVS - dysrhythmias, tachypnea
46
hypochloremia tx
- Treat underlying cause
* Alkalosis?
- Adequate hydration
47
hyperchloremia tx
- Treat underlying cause
* Acidosis?
- Limit NaCL
48
calcium functions
- 99% of body’s calcium forms the bones
- 1% found in the ECF
- Affects neuromuscular excitability
- Required for muscle contractions (heart,
skeletal)
- Affects coagulation
49
calcium regulation
- Parathyroid hormone – increases serum
calcium from bone breakdown
- Calcitonin – reabsorbs serum Ca++ to bones
- Kidneys excrete excess calcium
- excreted in feces
50
hypocalcemia causes
- Renal failure – Ca++ not reabsorbed
- PTH suppression – Ca++ not released from bone
- Malabsorption, decreased dietary intake
- Hyperphosphatemia
51
hypocalcemia manifestations
- Na+ moves into cells faster as calcium is
not blocking Na+
- Hyperreflexia, tetany, convulsions, cramps
- Chvostek and Trousseau signs
52
hypercalcemia causes
- Hypothyroidism
- Hyperparathyroidism
- Bone breakdown – tumors, metastasis
53
hypercalcemia manifestations
- Calcium prevents Na+ from entering
the cell as quickly -> decreased muscle/
neuron excitability
- Muscle weakness
- Cardiac Arrest
- Chronic – kidney stones
54
hypocalcemia tx
- Treat underlying cause
* Hyperphosphatemia – bind phosphate?
Dialysis?
Correct acid/base imbalance
- IV replacement – Ca Gluconate or CaCL (stronger)
55
hypercalcemia tx
- Treat underlying cause
* Hypophosphatemia
* Correct acid/base imbalance
- Dialysis (kidneys excrete Ca)
56
phosphate functions
- required for ATP formation
- found in ICF and bone
- maintains cell membrane stability
- acid base balance
- bone hardness
57
phosphate regulation
- absorbed GI system
- excreted/reabsorbed by kidneys
58
hypophosphatemia causes
- Malabsorption, decreased Vit D intake
- Antacid use (binds phosphate)
- ETOH
- Hyper-parathyoidism
59
hypophosphatemia manifestations
- Soft bones
- Muscle weakness
- Hypercalcemia symptoms
- Impaired plt aggregation
60
hyperphosphatemia causes
- Hypocalcemia
- Kidney failure
- Cell damage
61
hyperphosphatemia manifestations
hypocalcemia
62
hyperphosphatemia tx
- Limit oral PO4
- Decrease GI absorption with PO4-binding agents
- Dialysis in renal dysfunction
63
hypophosphatemia tx
- replace lost PO4 (IV or OG)
64
magnesium functions
- Assists with Na/K transport
- Helps Ca+ enter smooth muscles
- Maintains neuromuscular activity
- Co-enzyme for ATP production
65
magnesium regulation
- Competes with Ca+ for
reabsorption in the GI tract
- Excreted by kidneys and feces
66
hypomagnesium causes
-Malnutrition
- Poor absorption
- Loss of GI fluids
- Overuse of diuretic
67
hypomagnesium manifestations
- Neuromuscular overstimulation –
twitching, cramps, hyper-reflexia
- Dysrhythmias
68
hypermagnesium causes
- High intake
- Renal dysfunction
- Cell death
69
hypermagnesium manifestations
Neuromuscular depression – weakness, hypoactive reflexes
70
hypermagnesium tx
- Limit oral intake
- Dialysis
- Adequate volume to perfuse
kidneys
71
hypomagnesium tx
- Replace low Mg
- Increase oral intake
72
___ and ____ compete for binding sites on albumin
Ca and H
73
in acidosis, ___ falls and ____ goes up
calcium, ionized calcium
74
ph > 7.2
Compensatory
catecholamines may sustain reasonable CO
75
ph 7.2-7.1
- Decreased contractility
- Decreased CO
- Hypotension
- Pulmonary
vasoconstriction –
decreased gas exchange
related to dead space
- arterial vasodilation
76
ph < 7.1
- impact on the CVS system is life threatening
- Resistance to vasoactive
drugs
- Dysrhythmias
- Profound hypotension
- Hyperkalemia
77
hepatocytes
- major functional cells of the liver that perform metabolic, secretory,
and endocrine functions.
- Conjugate bilirubin
78
kupffer cells
- Make up 70% of bodies macrophages
- Line sinusoids
- Produce cytokines (triggered by endotoxins)
- Filter bacteria and endotoxins
- Destroy worn RBC, WBC, and bacteria
79
liver protein metabolism and synthesis of clotting factors
- Albumin (intravascular oncotic pressure)
- Globulins (immune function)
- Clotting factors
(fibrinogen, prothrombin & factors V, VII, IX & X)
- Converts amino acids to glucose or lipids
- Synthesizes amino acids
80
signs or symptoms of liver failure
- decreased LOC
- bleeding
- edema, ascites, leaking wound sites
- jaundice
- infection
- portal HTN
- hypoglycemia
81
AST
- Aspartate aminotransferase
- Found in liver, heart, skeletal muscles, kidneys and pancreas.
- LOW SPECIFICITY FOR THE LIVER
82
ALT
- Alanine Aminotransferase- Most ALT elevations are caused by liver damage. Its produced predominantly
in the liver and to a lesser extent the heart, kidneys, and skeletal muscle.
- HIGH SPECIFICITY FOR THE LIVER
83
what LFTs go up in all forms of recent injury? what must they be correlated with?
AST, ALT; correlate with pt condition and hx
84
albumin has a half life of ____ and is a good indicator for ____
20 days; chronic liver injury
85
____ is a very sensitive indicator of liver dysfunction
PTT, INR
86
GGT
very sensitive but non specific indicator of hepatobiliary disease.
DOES NOT ELEVATE IN BONE DISEASE.
87
ALK PHOSPH
TENDS TO BE
MORE SPECIFIC TO BONE DISEASE.
88
if alk phosph and ggt elevated
liver disease
89
if alk phosph up and ggt normal
bone related
90
a drop in ALT means
could mean hepatocytes are dying or theres improving function
91
hallmark signs of refeeding syndrome
- Hypophosphataemia
- Abnormalities of fluid balance
- Vitamin deficiency, e.g., vitamin B1 (thiamine)
- Hypomagnesaemia
- Hypokalemia
*lead to cardiac, resp, and neuromuscular consequences
