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Virtual Ward > N+V > Flashcards

N+V Flashcards

1
Q

List some of the neurological causes of vomiting.

A 
migraine
meningitis
stroke
raised ICP
vestibular disorders
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2
Q

Name endocrine causes of vomiting.

A 
diabetes
DKA
hypercalcaemia
thyroid disorders
Addisons disease
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3
Q

Name some GI causes of vomiting.

A 
infection
gastritis
gastroenteritis
obstruction
ileus
ischaemia
cancer
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4
Q

Discuss which drugs can cause vomiting.

A

side effects of digoxin, chemotherapy
poisoning
alcohol
cannabis

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5
Q

What gynaecological causes are there of vomiting?

A

pregnancy
malignancy
Torsion

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6
Q

A patient presents with a 2 day history of diarrhoea and vomiting. They note some bleeding when they wipe and you record a high temperature on obs. They tell you they think some of the kids in their children’s class have been off with tummy bugs. What is your first impression?

A

gastroenteritis

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7
Q

Paul presents to you with abdominal pain, constipation and episodes of vomiting. On examination you note his abdomen is distended, scars from past surgery and tinkling bowel sounds. What is your first impression and what investigations are you going to order?

A

bowel obstruction
AXR
CT

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8
Q

Fiona presents with severe epigastric pain and vomiting You see in her notes that she is a known alcoholic who has had gallstones in the past. What is your first impression and how will you investigate?

A

acute pancreatitis
amylase
USS

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9
Q

A 27 year old female presents with a history of vomiting and missed periods. What is your first impression and what investigations will you order?

A

pregnancy
urine bHGG
abdo/pelvic USS

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10
Q

How would a patient with ovarian cancer present and what investigations would you order?

A 
nausea and vomiting
abdominal pain
bloating
abdominal distention
ascites
weight loss
Ix: Ca125, pelvis USS, consider CT
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11
Q

What is hyperemesis gravidarum?

A

persistent vomiting and dehydration associated with pregnancy

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12
Q

Besides vomiting, what are the associated symptoms of migraine?

A

headache
aura symptoms
hyperacusis
photo/phono-phobia

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13
Q

How would meningitis present?

A

fever, headache, vomiting, rash, neck stiffness, meningism, reduced GCS

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14
Q

What are the symptoms of raised ICP?

A

headache, vomiting, blurred vision, reduced GCS, Cushings triad

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15
Q

A known type 1 diabetic presents with polyuria, polydipsia, N+V, abdo pain and appears confused. What is your main concern?

A

diabetic ketoacidosis

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16
Q

Define DKA.

A
  1. Glucose > 11 or known diabetes
  2. Acidosis: pH < 7.3 or bicarb < 15
  3. Ketones > 3 mmol/l or ++ on urine dip
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17
Q

What is the anion gap and how is it calculated?

A

The anion gap is a calculated difference between measured positively and negatively charged ions in your blood
([Na+] + [K+]) − ([Cl−] + [HCO−3])

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18
Q

What are the causes of a raised anion gap metabolic acidosis?

A 
Methanol
Uraemia
DKA
Palaldehyde
Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
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19
Q

What are the causes of a normal anion gap metabolic acidosis?

A

decreased acid excretion or loss of HCO3-

GI loss or renal disease

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20
Q

What are the principles of treatment for DKA?

A 
fluid replacement
insulin therapy
IV glucose therapy
correction of hypokalaemia
treatment of underlying triggers
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21
Q

Which fluids are generally given initially in DKA?

A

IV 0.9% NaCl

NB: risk of cerebral oedema if fluid is replaced too quickly

22
Q

Which initial insulin regime should you prescribe for a patient with DKA?

A

fixed rate IV insulin - commenced at 6 units/hour independent of BM within 30 minutes of admission or DHA diagnosis

23
Q

When and why should IV dextrose 10% be started?

A

When blood glucose falls below 14 mmol/L then IV dextrose 10% should be started aiming to keep blood glucose between 9-14 mmol/L, allows continuation of IV insulin and suppression of ketone formation

24
Q

What effect does DKA have on body potassium?

A

increased H+ ions and insulin deficiency results in whole body potassium deficiency despite normal serum K results

25
Q

What are the requirements for discontinuing the DKA pathway?

A 
eating and drinking
bicarbonate in normal range
ketones < 0.3
restarted on normal insulin regime
review by diabetes team
26
Q

What are the criteria for HHS?

A 
Laboratory glucose >30mmol/L
Venous blood gas [H+] <50nmol/L
Venous bicarbonate >15mmol/L 
Capillary blood ketones <3mmol/L (urine ketones <3+)
Serum osmolality >320mosmol/kg
27
Q

What is the first line management of HHS?

A

start 0.9% saline immediately
follow the HHS pathway and print out a copy for the notes
insert a catheter to monitor urine output

28
Q

What are some causes of HHS in diabetics?

A 
gastroenteritis
myocardial infarction
medications
substance abuse
stroke/TIA
29
Q

Are patients with DKA or HHS at higher risk of thromboembolism?

A

HHS - should receive prophylactic LMWH unless contra-indicated

30
Q

What are the three main characteristics of HHS?

A

hypovolaemia
marked hyperglycaemia without acidosis or hyperketonaemia
osmolality usually 320 mosmol/kg or more

31
Q

What are some intercurrent or co-existing illness which causes HHS?

A 
MI
infection
stroke/TIA/ICH
hyperthermia
hypothermia
intestinal infarction
pancreatitis
PE
AKI
hyperthyroidism
acute abdomen
Burns
Cushing
GI bleed
32
Q

Which medications can cause HHS?

A 
metformin during intercurrent illness
diuretics
BB
H2 receptor antagonists
dialysis
CC blockers
anti-psychotics
carbonic anhydrase inhibitors
glucocorticoids
phenytoin
substance misuse
33
Q

What are some diabetes-related causes of HHS?

A

first presentation

poor control - intentional, accidental, self-neglect, neglect or abuse by carers/family

34
Q

What is T1DM?

A

an autoimmune condition where insulin producing beta cells of the pancreas are destroyed by autoantibodies

35
Q

What is T2DM?

A

cells become resistent to actions of insulin - associated with obesity and inactivity

36
Q

Define diabetes mellitus.

A

chronic metabolic disease of hyperglycaemia as a result of insufficient insulin or resistance to its actions

37
Q

Discuss the physiology of insulin.

A

peptide hormone produced in the beta cells of the islets of Langerhands of the pancreas
secreted in response to blood glucose levels, reduced secretion as blood glucose levels fall
anabolid steroid which promotes glucose absorption into cells e.g. liver, muscle, fat
glucose converted to glycogen (glycogenesis) and fats (lipogenesis

38
Q

Discuss the presentation of T1DM.

A 
children/young adults
short history
polyuria/polydipsia/nocturia
fatigue
weight loss
personal or FHs of autoimmune disease
DKA
39
Q

How would you diagnose T1DM?

A

clinical signs and symptoms

hyperglycaemia i.e. random blood glucose > 11.1 mmol/l or fasting blood glucose > 7.0 mmol/l

40
Q

Name two rapid acting insulins.

A

novorapid

humalog

41
Q

Name two short acting insulins.

A

actrapid

humulin S

42
Q

Name two intermediate acting insulins.

A

isophane insulin

insulatard

43
Q

Name two long acting insulins.

A

levemir
lantus
tresiba

44
Q

Name two pre-mixed insulins.

A

novomix 30

humalog mix 25 or 50

45
Q

Name the three types of insulin regimes.

A

basal bolus
BD mixed insulin
continuous infusion

46
Q

Name some complications of T1DM.

A 
retinopathy
ESRF
poly/mono-neuropathy
PVD
thyroid, coeliac, Addisons disease
CVD
DKA
47
Q

What are some triggers of DKA?

A 
first presentation T1DM
infection
alcohol
MI
missed/insufficient insulin dose
48
Q

Discuss the pathophysiology of DKA.

A
  • trigger
  • insulin deficiency, increased counter regulatory hormones
  • glycogenolysis, gluconeogenesis, ketogenesis = hyperglycaemia
  • increased lipolysis, FFA formation = ketone body formation and acidosis
49
Q

How does DKA present?

A 
polydipsia
acetone breaht
Kussmaul breathing
N+V
abdominal pain
altered mental state
confusion
reduced GCS
dehydration
tachycardia
hypotension
dry mucus membranes
polyuria
glycosuria
ketonuria
50
Q

What are the complications of DKA?

A 
mortality 0.67%
VTE
arrhythmias
cerebral oedema
ARDS
AKI

Virtual Ward (11 decks)

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