1. Glucose > 11 or known diabetes 2. Acidosis: pH 3 mmol/l or ++ on urine dip

N+V Flashcards by Sarah Kennedy

List some of the neurological causes of vomiting.

migraine
meningitis
stroke
raised ICP
vestibular disorders

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Name endocrine causes of vomiting.

diabetes
DKA
hypercalcaemia
thyroid disorders
Addisons disease

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Name some GI causes of vomiting.

infection
gastritis
gastroenteritis
obstruction
ileus
ischaemia
cancer

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Discuss which drugs can cause vomiting.

side effects of digoxin, chemotherapy
poisoning
alcohol
cannabis

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What gynaecological causes are there of vomiting?

pregnancy
malignancy
Torsion

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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?

gastroenteritis

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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?

bowel obstruction
AXR
CT

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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?

acute pancreatitis
amylase
USS

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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?

pregnancy
urine bHGG
abdo/pelvic USS

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

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

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What is hyperemesis gravidarum?

persistent vomiting and dehydration associated with pregnancy

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Besides vomiting, what are the associated symptoms of migraine?

headache
aura symptoms
hyperacusis
photo/phono-phobia

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How would meningitis present?

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

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What are the symptoms of raised ICP?

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

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

diabetic ketoacidosis

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Define DKA.

Glucose > 11 or known diabetes
Acidosis: pH < 7.3 or bicarb < 15
Ketones > 3 mmol/l or ++ on urine dip

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What is the anion gap and how is it calculated?

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

Methanol
Uraemia
DKA
Palaldehyde
Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates

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

decreased acid excretion or loss of HCO3-

GI loss or renal disease

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What are the principles of treatment for DKA?

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

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Which fluids are generally given initially in DKA?

IV 0.9% NaCl

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

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

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

When and why should IV dextrose 10% be started?

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

What effect does DKA have on body potassium?

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

What are the requirements for discontinuing the DKA pathway?

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

What are the criteria for HHS?

``` 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 ```

What is the first line management of HHS?

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

What are some causes of HHS in diabetics?

``` gastroenteritis myocardial infarction medications substance abuse stroke/TIA ```

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

HHS - should receive prophylactic LMWH unless contra-indicated

What are the three main characteristics of HHS?

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

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

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

Which medications can cause HHS?

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

What are some diabetes-related causes of HHS?

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

What is T1DM?

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

What is T2DM?

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

Define diabetes mellitus.

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

Discuss the physiology of insulin.

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

Discuss the presentation of T1DM.

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

How would you diagnose T1DM?

clinical signs and symptoms | hyperglycaemia i.e. random blood glucose > 11.1 mmol/l or fasting blood glucose > 7.0 mmol/l

Name two rapid acting insulins.

novorapid | humalog

Name two short acting insulins.

actrapid | humulin S

Name two intermediate acting insulins.

isophane insulin | insulatard

Name two long acting insulins.

levemir lantus tresiba

Name two pre-mixed insulins.

novomix 30 | humalog mix 25 or 50

Name the three types of insulin regimes.

basal bolus BD mixed insulin continuous infusion

Name some complications of T1DM.

``` retinopathy ESRF poly/mono-neuropathy PVD thyroid, coeliac, Addisons disease CVD DKA ```

What are some triggers of DKA?

``` first presentation T1DM infection alcohol MI missed/insufficient insulin dose ```

Discuss the pathophysiology of DKA.

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

How does DKA present?

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

What are the complications of DKA?

``` mortality 0.67% VTE arrhythmias cerebral oedema ARDS AKI ```