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CICM > Acid Base > Flashcards

Acid Base Flashcards

1
Q

Delta ratio

A

Used to determine if there are multiple processes in met acidosis

Change in AG/change in bicarbonate

<0.4 - NAGMA
0.4-0.8 - mixed
1-2 - HAGMA
>2 - HAGMA with pre-existing met alkalosis

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2
Q

Urinary AG

A

Na + k - cl

Differentiate between renal and GI cause for NAGMA

Renal causes - increased (due to increased urinary bicarb)
GI causes - decreased (due to increased ammonia secretion)

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3
Q

Base excess vs standard base excess

A

BE - dose of acid or base required to return the pH to 7.4 of a while blood sample, at 37 deg, PaCO2 40 (isolates the metabolic disturbance from the respiratory)

standard base excess -
dose of acid or base required to return the pH of an anaemic blood sample to 7.4, calculated for Hb 50g/l
- assesses the buffering of whole extracellular blood, not just Hb rich intravascular fluid

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4
Q

Normal SBE with abnormal anion gap -

A

HAGMA with pre-existing met alkalosis

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5
Q

Negative SBE with normal anion gap

A

anion gap uncorrected for a low albumin

NAGMA

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6
Q

Boston rules - acute resp acidosis

A

For every 10mmHg rise in PaCO2 the bicarb will increase by 1

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7
Q

Boston rules - chronic resp acidsis

A

for every 10mmHg rise in PaCO2 the bicarb will rise by 4

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8
Q

Boston rules - Acute resp alkalosis

A

for every 100mmHg decrease in PaCo2 the bocarb will fall by 2

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9
Q

Boston rules - metabolic acidosis

A

PacO2 = (1.5x bicarb) + 8

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10
Q

Boston rules - met alkalosis

A

PaCo2 = (0.7 x bicarb) + 20

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11
Q

Causes of rasied Anion gap

A 
Ketoacidosis - alcohol, starvation, diabetic
Metformin
uraemia
pyroglutamic acidosis
iron, isoniazid
lactate
ethylene glycol
salicylates
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12
Q

Osmolal gap

A

scans for unmeasured osmotically active molecules
difference between measured and calculated osmolality

normal gap is <10mOsmol/kg

Causes of raised gap

  • methanol
  • etylene glycol
  • manninol
  • glycine
  • acetone
  • glycerol
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13
Q

Causes of normal anion gap and high osmolar gap

A

Any substance administered into bloodstream which does not dissociate into bloodsream to change pH

Mannitol
glyceine
non-metabolised glycols
maltose
ethanol

Albumin (falsely normal AG)

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14
Q

Causes of high anion gap and high osmolar gap

A

Endocrine and metabolic causes -

  • lactate
  • alcoholic or diabetic ketoacidosis
  • acute kidney injury

Toxicological causes -

  • methanol intoxication (anion is formic acid)
  • ethylene glycol (anions are glycolic and oxalic acid)
  • salycilate (anions are salycilate and lactate)
  • any toxin causing a massive lactic acidosis 0 eg isoniazid
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15
Q

Causes of high anion anion gap and normal osmolar gap

A

abnormally large value of albumin

late stage toxic alcohol intoxication (the extra osmoles have been metabolised)

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16
Q

Clinical features of acidosis

A

Most severe at pH <7.2 (7.15 when try to correct)

Reduced myocardial contractility, arrythmias, systemic arteriolar dilatations, venoconstriction, centralisation of blood volume

Pulmonary vasoconstriction, hyperventilation, respiratory muscle failure

Reduced splanchnic tone and renal blood flow

Increased metabolic rate, catabolism, reduced ATP synthesis

Conusion, drowsiness

Increase iNO expression, pro-inflammatory cytokine release

Hyperglycaemia, hyperkalaemia

Cell membrane pump dysfinction

Bone loss, muslce wasting

17
Q

specific issues with formate

A

blindness and cerebral oedema

18
Q

specific issues with oxalate

A

crystalluria, renal failure, hypercalcaemia

19
Q

specific issues with salycilate

A

tinnitus, hyperventilation and fever due to uncoupling of oxidative phosphorylation

20
Q

Approach to metabolic acodisis

A

Anion Gap - ?unmeasured anions, if normal - changes in bicarb or chloride are the cause

Delta ration - quantifies the conribution of anions and chloride/bicarb to the change in pH
- can identify mixed diosrders

Urine anion gap (for NAGMA) -
high - renal cause
low or negative - GI

Caculate osmolar gap (for HAGMA)

21
Q

Causes of NAGMA

A

CAGE

CHloride
acetazolamide/addisions
GI loss - diarrhoea, fistulae, ureteroenterostomies, pancreatoenterostomies
Extras - RTA, recovery phase of DKA

22
Q

RTA types

A

Type 1 -
- distal - continues to resporb cl despite acidosis
- severe acidosis
- severe hypOK
- urine very alkaline
Causes - autoimmune disease, hyperCa conditions, post renal Tx, wilsons disease, drugs - cyclophosphamide

Type 2 -

  • proximal - interefence with bicarb resorption (bicard is excreted when it shouldn’t be)
  • moderate acidosis
  • moderate hypOK
  • caused by fanconi syndrome, amyloid, light chain disease, drugs - lead, acetazolamide
  • need huge intake of bicarbinate to correct

Type 4 - hypoaldosteronism/hypoadrenalism cause metabolic acidosis by causing loss of renal sodium and decreasing chloride secretion
- mild acidosis
- hypERK
Causes
- failure of renin secretion
- angiotensin system failure - ACEi, ARBs, heparin
- decreased aldosterone secretion - primary hypoaldosteronism, prin=mary adrenal insufficiency, steroids, NSAIDS, critical illness
- aldosterone receptor malfunction - calcineurin inhibitors (tacro), spinonolactone
- ENaC Na channel blockade (aldosterone responsive epithelial Na channel) - amiloride, trimethoprim

Treated with synthetic mineralicorticoid eg fludrocortisone

23
Q

Types of lactic acidosis

A

A - impaired tissue oxygention
- shock, regional ischaemia, severe hypoxia, severe anaemia, carbon monoxide poisoning

B1 - due to disease state
- malignancy, thiamine deficiency, ketoacidosis, HONK, spetic shock, impaired hepatic or renal clearance

B2 - drug induced

  • beta2 adrenoceptor agonists
  • metformin
  • cyanide
  • isoniazid
  • propofol
  • toxic alcohols eg methanole
  • salycilates

B3 - inborn errors of metabolism

  • pyruvate dehydrogenase deficicney
  • electron transport chain defects
  • G6PD
24
Q

Causes of raised lactate in sepsis

A

endogenous catecholamine release and administration of infusions

circulatory failure due to hypoxia and hypotension

microvascular shunting

inhibition of pyruvate dehydrogenase by endotoxin

coexistant liver disease

slowed hepatic blood flow, impairment clearance

25
Q

D lactate

A

produced by bacteria in the colon and usually we can metabolise large amounts

D lactate is not routinely measured, and so may be a cause of a HAGMA with ‘normal’ lactate

Present with neurological symptoms - confusion, slurred speech, obtundation, ataxia

Risk factors -

  • short gut
  • post-pancreatectyom who dont take enzyme supplements
  • patients to take extra lactobacillus
  • symptoms are exacerbated by food intake (cardbohydrate is fermented -> D lactate)
26
Q

Pyroglutamic acidosis

A

rare, but lots of SAQs

occurs due to glutathione depletion in patients who are already glutathione deplete

Mechanism -
- pyroglutamic acid is produced by an enzyme that is stimulated with low glutathione stores -> accumulation of pyroglutamic acid

May be depleted by
- sepsis
- paracetamol
chronically by - liver disease and malnutrition

Diagnosis depends on detection of 5-oxoproline (urinary or serum level)

Risk factors -

  • paracetamol
  • sepsis
  • chronic alcohol/liver failure of any cause
  • old age
  • weird diet/malnutriotn
  • flucloxacillin, vigabatrin (cause dysfunction of 5-oxoprolinase)
  • renal failure

Mx -

  • cessation of causative agent (if present)
  • NAC
27
Q

Pathophysiology of ketoacidosis

A

genertion of ketones is normal response to fasting (following depletion of hepatic glycogen stores)

In glucose-poor environment - too much oxaloacetate is diverted away into gluconeogenesis
-restricts entry of acetyl-coA in to Krebs cycle -> diverted in ketogenesis

Also an increase in beta-oxidation of fatty acids (lipolysis)

Starvation -> decreased insulin and increased lipolysis -> increased delivery of FFAs to liver which exceeds capacity of ACoA to enter krebs cycle -> ketogenesis

28
Q

Types of ketoacidosis

A

starvation (after 3 days) - due to decreased intake of carbs, decreased insulin. Ketogensis due to inadequate glycogen stores

  • mild acidosis
  • low ketones
  • BSL low
  • concerns about refeeding sydrome

Alcoholic - starvation following a binge

  • hepatic metabolism of ethanol depletes NAD and increases NADH -> favours converstion of acetoacetate to beta hydroxybutyrate
  • moderate acidosis, low BSL

Diabetic
- absence of insulin and presence of stress hormones/glucagon -> hepatic lipid metabolism switches to ketogenesis

29
Q

Toxic alcohols

A

contribute to HAGMA by being metabolised
Alcohol dehydrogenase is the enzyme common to all
- if this is blocked, the alcohols are benign (and are excreted rapidly via kidneys)

Ethanol -> acetate

Methanol -> formate

Ethylene glycol -> glycolic acid
- one mouthful is enough
- stages 1) intoxication (high AG but no acidosis) 2) coma and seizures with metabolic acidosis 3) cardiac toxicity
- key diagnostic feature is calcium oxalate crystals
Management - bicarbonate and alcohol (to overwhelm alcohol dehydrogenase), fomepiozole, dialysis

30
Q

Ethylene glycol treatment

A

bicarbonte
Ethanol
fomepizole (competitive anatagonist to alcohol dehydrogenase)
Dialysis - main indication is high osmolar gap

31
Q

Causes of metabolic alkalosis

A

Exogenous strong cation excess -

  • Na bicarb or citrate
  • beta lactam
  • hypercalcaemia

Primary derangement of homeostatic mechanisms -

  • failure of bicarb in ESRF
  • hypoalbuminaemia

Enteric chloride depletion -
- gastric loss or loss due to villious adenoma

Renal chloride depletion -

  • diuretic induced
  • post hypercapnic state
  • Bartters and Gitelmmans, cyctic fibrosis
  • hypokalaemia, HypoMg

Mineralocorticoid excess -

  • renin secreting adenoma
  • RAS
  • primary hyperaldosteronism
  • steroid administration/cushings
32
Q

How to determine cause of met alk

A 
History - ?beta lactams, steroids, CF
Urinary chloride
Blood pressure trends
Serum renin levels
Serum aldosterone levels
33
Q

Causes of respiratory acidosis

A

Increased inspired fraction of CO2

Decreased alveolar ventilation (increases by 3mmHg for each minute of apnoea)

Increased metabolic CO2 production

34
Q

Calculation of bicarb dose

A

body weight x 0.3 x SBE

body weight x0.3 x (desired bicarb - measured bicarb)

35
Q

Adverse effects of Na bicarb

A 
phlebitis
hyperNa
volume overload
HypOK
ionised hypOCa
left shift of ODC
impaired clearance of lactate
intracellular acidosis (maybe)
hypercapnea
36
Q

ABG changes in pregnancy

A 
increased pH
decreased CO2
increased O2
decreased bicarb
2.3DPG increases
p50 remains the same becuase of the alkalosis

CICM (20 decks)

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