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GI > Consequences of Fluid Loss from GIT > Flashcards

Consequences of Fluid Loss from GIT Flashcards

1
Q

Total body water balance?

A 
Intake (volumes)
Liquids: 1200ml
Food: 1000ml
Metabolically produced: 350ml
Total: 2550ml
Output (volumes)
Insensible water loss -  by transepidermal diffusion, evaporates via skin +respiratory tract 900ml
Sweat: 50ml
Faeces: 100
Urine: 1500
Total: 2550ml
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2
Q

Sites of water loss?

A 
Skin
Respiratory passageways
GIT
Urinary tract
Menstrual flow
Trauma
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3
Q

Total balance of Na + Cl?

A 
Excretion small, but large in diarrhoea, sweating, vomiting, haemorrhage → loss of water + salts
-Intake (grams):
Food: 10.5g
-Output (grams):
Sweat: 0.25g
Faeces: 0.25g
Urine: 10.00g – varies
Total output: 10.5g
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4
Q

Ways in which fluid is lost + gained?

A 
-Water loss:
Defecation; diarrhoea
Vomiting: what is lost?
Urination
Ventilation
Sweating
Menstruation

-Water gain:
Drinking
Metabolic

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5
Q

Features of diarrhoea?

A
  • ↑Frequency, with ↑volume + fluidity of faeces
  • > 3 Unformed stools per 24hrs
  • Change in bowel movement
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6
Q

Why does diarrhoea occur?

A
  • Failure of water absorption

- ↑Secretion or both

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7
Q

Causes of decreased absorption?

A
  • ↑Osmotic particles (osmotic diarrhoea)
  • ↑Rate of flow of intestinal contents (deranged motility diarrhoea)
  • Abnormal increase in secretions of GIT (secretory diarrhoea)
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8
Q

Why does osmotic diarrhoea occur?

A

excess water drawn into the bowels when drink solutions with excessive or salt it draw water from body into bowel

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9
Q

Effect of osmotic diarrhoea?

A
  • Decreased absorption of electrolytes + nutrients

- Disaccharidase def (disaccharide def/malabsorption), drug-induced, malabsorption of galactose)

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10
Q

Effect of inflammatory bowel disease?

A

chronic exudative diarrhoea

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11
Q

Cause of traveller’s diarrhoea?

A

bacteria

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12
Q

Features of secretory diarrhoea?

A
  • ACh, sub P, 5-HT, neurotensin act via ↑[Ca2+] to increase rate of intestinal secretion
  • Excessive laxative use, defects in digestion + absorption infections eg cholera Vibrio cholerae) :
  • survives acidic conditions of gut
  • enterotoxin stimulates adenylate cyclase → ↑cAMP → Na+, Cl- + water loss
  • Replace water, electrolytes, glucose (treatment)
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13
Q

Features of deranged motility diarrhoea?

A
  • Lack of absorption - some agents promote secretion + motility
  • GI stasis promote diarrhoea by stimulating bacterial overgrowth
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14
Q

Parasitic causes of diarrhoea?

A
  • Entamoeba histolytica + Giardia lamblia
  • Entamoeba histolytica :
  • Asymptomatic or amoebic dysentery
  • Gradual in onset → systemic symptoms (anorexia, headache)
  • Metronidazole
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15
Q

Features of giardia?

A
  • Steatorrhoea + abdominal pain - maldigestion + malabsorption of lipids, CHOs, vit A, vit B12, folic acid
  • Metronidazole or tinidazole
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16
Q

What’s dysentery?

A

painful, bloody, low volume diarrhoea

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17
Q

Causes of bloody diarrhoea?

A

Chronic disease
Ulcerative colitis
Neoplasm
Stress

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18
Q

Consequences of excessive loss of water, nutrients, Na+, K+, HCO3-?

A
  • ↓Blood volume (hypovolaemia)

- Metabolic acidosis – due HCO3- loss in diarrhoea

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19
Q

Decsribe how volume depletion leads to acidosis/alkalosis

A
  • severe diarrhoea (eg from laxative abuse or renal loss of K+ from kidney prob cause less HCO3- to neutralise acids in blood)
  • alkaline secretions into large + small bowel with bicarb level > plasma
  • excessive loss of fluids –> normal anion gap metabolic acidosis
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20
Q

Features of vomiting?

A

=Retrograde giant contraction, oral expulsion of gastric contents + bile

  • Symptom of illness (children)
  • Pregnancy
  • Alcohol dependency
  • Metabolic disorders eg uraemia (fluid + electrolyte imbalance, CKD)
  • Allows removal of ingested toxic substances
  • ↑ salivation,
  • ↑ heart rate
  • ↑ sweating
  • Pallor
  • Nausea- allows avoidance of toxic substances in future
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21
Q

Features of uraemia?

A
  • Clinical syndrome associated with fluid, electrolyte, hormone imbalances, metabolic abnormalities which develop in parallel with deterioration of renal function
  • Develops with chronic kidney disease (CKD)
  • Occur with acute kidney injury (AKI) if loss of renal function is rapid
  • Toxins : parathyroid hormone (PTH), beta2 microglobulin, polyamines, advanced glycosylation end products, other middle molecules contribute
  • Complications : seizure, coma, cardiac arrest, death, spontaneous bleeding, GI bleeding, spontaneous subdural hematomas, increased bleeding from any underlying disorder, bleeding associated with trauma, cardiac occur from severe underlying electrolyte abnormalities eg hyperkalaemia, metabolic acidosis, hypocalaemia
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22
Q

What controls vomiting?

A
  • Brainstem medulla oblongata is vomiting centre
  • Neuronal inputs from body to brainstem stimulates vomiting reflex
  • Chemoreceptor trigger zone
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23
Q

Inputs that initiate vomiting?

A
  • Distension of stomach or small intestine
  • Action of substances on chemoreceptors in brain or intestine
  • ↑Pressure in skull
  • Rotating movements of head (motion sickness)
  • Intense pain
  • Tactile stimuli to the back of the throat (gag reflex)
  • Sight, smell, emotional circumstances
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24
Q

Describe process of vomiting

A
  • nausea (sweating, pallor, hypersalivation)
  • deep inspiration (closure of epiglottis)
  • ↑abdominal pressure
  • retrograde giant contraction
  • breath held, chest fixes
  • ↓oesophageal pressure
  • relaxation of oesophageal sphincters
  • ↑abdominal pressure
  • forceful expulsion
  • retching
  • bile expelled (contraction of upper portions of intestine)
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25
Q

What’s radiation colitis?

A

inflammation of colon as side effect of cancer radiation therapy to abdomen or pelvis

26
Q

How do 5-HT antagonist drugs (ondansetron) work?

A
  • prevents serotonin so…
  • prevents transmission of vomit signal via nerves from intestines to brain
  • prevents stimulation of vomiting centre
27
Q

Consequences of excessive vomiting?

A 
↑Salt + water loss
Severe dehydration
Circulatory problems
Metabolic alkalosis – due to loss of gastric acid (HCl)
Nutritional deficit – failure to thrive
Death
28
Q

What’s lost in vomit?

A 
Food
Mucus with Na+, K+, Cl-, HCO3-
Gastric acid
Upper intestinal contents (incl. bile)
Blood
29
Q

Consequences of fluid loss from GIT?

A

Hypovolaemia
Haemoconcentration/polycythaemia (dehydration) =↑[RBC]
Dehydration
Ionic imbalances; poor perfusion of tissues
Malnutrition + ↑mortality

30
Q

Describe consequences of hypovolaemia

A
  • ↓venous return
  • arterial hypotension
  • myocardial dysfunction due ↑myocardial oxygen demand + ↓tissue perfusion
  • ↑anaerobic metabolism
  • acidosis + myocardial dysfunction → multi-organ failure
31
Q

What’s polycythaemia?

A

=erythrocytosis

  • High conc of 🔴 in blood
  • Blood thicker + can’t travel through blood vessels+ organs
  • Sluggish flow of blood
32
Q

Signs + symptoms of polycythaemia?

A

headcahe
blurred vision
red skin, particularly in the face, hands and feet
tiredness
high blood pressure
dizziness
discomfort inthe tummy (abdomen)
periods of confusion
bleeding problems– nosebleeds + bruising
gout - cause joint pain, stiffness, swelling
itchy skin– after bath due to white blood cells releasing histamine

33
Q

What’s haemoconcentration?

A

Decrease in plasma volume in relation to number of 🔴 –> increase in 🔴 conc in circulating blood

34
Q

Why’s hypotension caused by hypovolaemia?

A

Haemorrhage; insufficient fluid intake, starvation or excessive fluid losses from diarrhea or vomiting
induced by excessive use of diuretics
Low blood pressure may also be attributed to heat stroke

35
Q

Indicators of hypovolaemia?

A

Absence of perspiration, light headedness, dark coloured urine

36
Q

Consequences of dehydration?

A
  • Water controls body temp : heat shock, headache, fainting, death
  • Heart works harder : higher blood viscosity (reduced circulation), higher BP, blood clotting
  • Digestion : constipation, acid reflux, indigestion, toxins accumulate, reduced nutrients
  • Kidneys overloaded : toxins accumulate + not flushed –> damaged kidney
  • Brain priority : takes water from body when thirsty
  • Skin with decreased turgor remains elevated after being pulled up + released

Nausea, headache, irrationality, cramps, ↑temp,dizziness

37
Q

Body’s response to water loss?

A
  • Cardiovascular adaptation
  • Renal adaptation
  • Behavioural stimulates fluid intake
38
Q

Features of renal arteries?

A
  • carry blood from heart to kidneys
  • branch directly from aorta on either side + extend to eachkidney
  • take large volume of blood to kidneys to be filtered before systole
39
Q

Describe physiologic response to hypovolaemia from diarrhea

A

-↑Na+ and H2O loss due to diarrhoea
-↓plasma volume
-↓venous pressure
-↑ activity of renal symp nerves mediated by venous baroreceptors
CVS adaptions :
*↓ venous return
*↓ atrial pressure
*↓ ventricular end-diastolic volume mediated by atrial baroreceptors
*↓ SV
*↓ CO
*↓ arterial BP
-↑ activity of renal symp nerves mediated by venous baroreceptors
-Renal adaptations :
*↑ constriction of renal arterioles
*↓ net glomerular filtration pressure to allow more time for reabsorption
*↓GFR
-↓ Na+ and water secretion

40
Q

Describe water loss by sweating + physiological adaptations

A
  • sweating
  • loss of hypo-osmotic salt solution
  • ↓ plasma volume + ↑ plasma osmolarity (↓H2O conc) :
  • ↓ plasma volume –> ↓GFR + ↑plasma aldosterone –> ↓Na excretion
  • ↑ plasma osmolarity (↓H2O conc) and ↓ plasma volume –> ↑ plasma ADH –> ↓H2O excretion
41
Q

Describe response to hypovolaemia via RAAS cascade

A

↓Plasma volume (↑Na+ and H2O loss) ↑plasma K+ :

  • Activity of renal symp nerves
  • ↓GFR so less flow to macula densa
  • Less arterial pressure
  • Activity of renal symp nerves via intrarenal baroreceptors causes renal juxtaglomerular cells to increase renin secretion ……..
  • ↓GFR so less flow to macula densa decreasing NaCl conc in macula densa causes renal juxtaglomerular cells to increase renin secretion ………
  • less arterial pressure causes less stretch
  • renal juxtaglomerular cells to increase renin secretion……
  • increases plasma renin
  • increases plasma Ang II
  • adrenal cortex increases aldosterone secretion
  • increases plasma aldosterone
  • cortical collecting ducts increase Na+ reabsorption and K+ loss
  • less Na+ excretion and increased K+ excretion
42
Q

Effect of macula densa sensing [NaCl]fluid passing?

A
  • ↓[NaCl] causes
  • ↑renin release
  • ↓resistance to BF in afferent arterioles via vasodilation
  • normal GFR
43
Q

Features of macula densa?

A
  • Closely packed specialised cells lining wall of cortical thick ascending limb at transition to distal convoluted tubule
  • Near end of ascending loop of Henle, distal convoluted tubule
  • Cells of macula densa sensitive to [NaCl] in late thick ascending limb
  • Decrease in [NaCl] initiates signal from macula densa resulting in :
  • ↓resistance to BF in afferent arterioles via vasodilation, which increases glomerular capillary hydrostatic pressure + helps return GFR normal
  • ↑renin release from juxtaglomerular cells of afferent + efferent arterioles
  • Increase in [NaCl] –> vasoconstriction of afferent arterioles, reduced paracrine stimulation of juxtaglomerular cells
  • Macula densa feedback, where compensatory mechanisms act to return GFR to normal
44
Q

What controls ADH release?

A

Osmoreceptors and baroreceptors

45
Q

Physiologic response to the consequences of hypovolaemia?

A
  • ↓ plasma volume
  • ↓ venous, atrial, arterial pressures mediated by cardiovascular baroreceptors
  • posterior pituitary ↑ADH secretion
  • ↑ plasma ADH
  • collecting ducts ↑tubular permeability to H2O
  • ↑ H2O reabsorption
  • ↓ H2O excretion
46
Q

How ADH regulates water loss?

A
  • stimulates thirst mechanism

- increased osmolarity of body fluids → ADH release

47
Q

How does ADH work?

A
  • inserts water channels (aquaporin-2) in collecting duct of kidney
  • increases permeability of collecting ducts to H2O
  • so con urine production
  • intake of plain H2O ↓ in osmolarity of blood + interstitial fluid
  • decreases ADH secretion + removal of water channels
  • if no water channels then decreased permeability of collecting ducts to water + increased water loss
48
Q

What’s osmolarity?

A

how conc solution is - total number of solute particles per litre of solution.

49
Q

Factors that regulate ADH release?

A
  • Decrease in blood volume (detected by baroreceptors)*
  • Dehydration –> GFR decreases causing less H2O in urine*
  • Excess intake of water –>high BP –> increased GFR + increased H2O in urine
  • Hyperventilation –> increased fluid loss (exhalation)*
  • Vomiting/diarrhoea –> increased fluid loss from GIT*
  • Fever, heavy sweating, burns –> large H2O loss*

*ADH secretion in leads to conservation of body H2O

50
Q

Effect of thirst centre in hypothalamus?

A

stimulates desire to drink –>water gain if thirst quenched

51
Q

Effect of Ang II?

A

Stimulates secretion of aldosterone –> decreases loss of H2O in urine

52
Q

Effect of aldosterone?

A

Promotes reabsorption of Na+, Cl-, H2O –> decreased water loss in urine

53
Q

Effect of ANP?

A

Stimulates natriuresis; increased excretion of Na+, Cl-, H2O –> increased loss of water in urine

54
Q

Effect of ADH?

A

inserts water channels in collecting ducts so increases permeability of collecting duct to water, improves its reabsorption –> decreased loss of water in urine

55
Q

Role of metering of water intake by GIT?

A

avoids over-rehydration

56
Q

Features of thirst?

A
  • Drive us to seek waterstimulated by lower extracellular volume + higher plasma osmolarity
  • Osmoreceptors + baroreceptors control ADH release identical to those for thirst
  • Brain centres receive input from receptors, mediate thirst located in hypothalamus, close to area that produces ADH
57
Q

Effect of Ang II injected into brain?

A

↑water intake + slow in NaCl intake occurs. Drinking is vigorous, highly motivated, rapidly completed

58
Q

Features of metering of water intake by the GIT?

A
  • If thirsty then drinks water, stops drinking after replacing lost water but before most water absorbed from GIT + eliminate stimulatory inputs to systemic baroreceptors, osmoreceptors
  • Avoid over-rehydration
  • Dryness of mouth + throat –> thirst
59
Q

How dehydration affects calcium levels?

A
  • dehydration
  • imbalance of electrolytes in bloodstream
  • ↓ NaCl and K+ and ↑[Ca2+]
  • ↑ [Ca2+] → hypercalcaemia
  • ↑ risk of kidney stones, kidney failure, arrhythmia
60
Q

Symptoms of hypercalcaemia?

A 
If mild= asymptomatic
Nausea
Vomiting
Loss of appetite
Constipation
Abdominal pain 
Excessive thirst
Fatigue, lethargy, muscle weakness
Joint pain, confusion

GI (15 decks)

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