Poisoning and DKA Flashcards by Tadah M

State 5 situations to suspect poisoning

Seizures
Altered mental state
Unexplained coma
Compromised CVS
Metabolic abnormality
Unstable patient

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What to ask in history of poisoned child x5

Type and amount of substance
Time and route of exposure
Time of symptom onset
Past medical history
Known drug allergies

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Most common types of agents in poisoning x6

Cosmetics
Analgesics
Foreign bodies
Plants
Self care products
Cleaning solutions

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Routes of poisoning x5

Ingestion
Inhalation
Parenteral -through injections
Ocular and dermal exposure
Mucous membrane involvement

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Ocular signs in poisoning and the causes x4

Miosis- organophosphates, muscarinic mushrooms
Mydriasis- antihistamines, cyclic antidepressants
Nystagmus- ethanol, phenytoin
Lacrimation- Organophosphates, irritant gas

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Oral signs in poisoning and the causes x5

Burns and dysphagia- corrosives
Dry mouth- antihistamines and anticholinergics
Salivation- organophosphates, corrosives
Hematemesis- corrosives, NSAIDs

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Causes of diaphoresis(sweating) and diarrhea in poisoning x3

Diaphoresis- Organophosphates, muscarinic mushrooms, aspirin
Diarrhea- Antimicrobials, iron, cholinergics

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3 respiratory signs in poisoning and their causes 3x2

Increased - asiprin and CO
Decreased- alcohol, narcotics
Pulmonary edema- hydrocarbons and organophosphates

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3 Cardiac signs in poisoning and their causes x2

Tachycardia- atropine, cyclic antidepressants
Bradycardia- B blockers, CA channel blockers
Hypotension- barbiturates, iron + above

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CNS effects of poisoning 5x2

Ataxia- alcohol, narcotics
Coma- sedative, CO
Muscle rigidity - haloperidol, cyclic antidepressants
Muscle fasciculation- organophosphates, theophylline
Peripheral neuropathy- organophosphates

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State 5 complications of poisoning

Coma
Toxicity
Seizures
Metabolic acidosis
GIT symptoms
Heart rhythm aberrations/diversions

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Differential diagnosis for coma x5

Asphyxia
Meningitis
Encephalitis
Cerebral malaria
Cerebrovascular accident

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Describe direct toxicity from hydrocarbons ingestion and aspiration

Emesis increases the risk of pulmonary toxicity
Hydrocarbons with low viscosity and surface tension increase the risk of aspiration pneumonia

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State 2 positions to open the airway and the age group

Neutral- <1 year
Sniffing- >1 year

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Airway assessment x3

Look- chest movement
Listen- air mvt and stridor
Feel- air mvt

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State 4 signs of increased work of breathing

Nasal flaring
Head nodding
Chest wall indrawing
Unable to eat or breastfeed

Management of shock x4

Stop bleeding
Give oxygen
Obtain IV access
Keep child warm

Stage 4 signs of seizure or convulsions

Increased tone
Eyes deviated
Facial twitching
Abnormal repetitive movement

State 5 triggers of DKA

Infarction
Infection
Intoxication
Intercurrent illness
Inappropriate withdrawal of insulin

Describe 2 liver effects of low insulin in the blood

Increased lipolysis > FFA> increased ketogenesis in the liver
Increased glucose production > hyperglycemia

Clinical features of DKA x5

Polyuria, polydipsia, abdominal pains, arrhythmias, N&V

State 4 effects of high plasma insulin

Glucose uptake
Glucose oxidation
Protein and glycogen synthesis

State 3 stress hormones secreted during insulinopaenia and their 2 functions

Glucagon, cortisol, epinephrine
1. To increase mobilization of energy source
2. Adapt individual to new circumstances

State short term 4 effects of insulinopaenia

Hyperglycemia
Lipolysis/ impaired lipid synthesis
Production of ketone bodies
Glycosuria, ketonuria, cations in urine

State 5 end effects of insulinopaenia

Acidosis Hyperosmolarity Progressive dehydration Diminished cerebral oxygen utilization Impaired consciousness and coma

Describe electrolyte imbalance in DKA x3

Potassium- hypokalemia caused by increased K+ in ECF > excretion Phosphate- buffering to increase renal excretion of H+ Sodium- osmotic diuresis + vomiting > dehydration

3 signs of intravascular volume depletion

Tachycardia Poor peripheral perfusion Decreased skin turgor

Define severe DKA x3

pH<7.15 CO2 <10 Kussmaul respirations, sleepy to depressed sensorium to coma

2 reasons why RL is preferred instead of NS in DKA

NS contains Na which increases dehydration RL contain K which corrects hypokalemia

Present and absent processes in the liver when there is high plasma insulin x5

Glucose uptake Glycogen synthesis Lipogenesis Absence of gluconeogenesis Absence of ketogenesis

State what happens in the liver when there’s no plasma insulin x5

Glucose production Glycogenolysis Absence of lipogenesis Gluconeogenesis Ketogenesis

Complications of diabetes x3

Retinopathy Renal dysfunction ie nephropathy Hypertension and hypercholesterolemia

When to use bicarbonate in DKA and 3 side effects

Only used in severe acidosis or symptomatic hyperkalemia 1. Crosses BBB and increases cns acidosis 2. Shifts oxyhemoglobin dissociation curve and causes hypoxia 3. Increased risk of cerebral edema

Risk factors of cerebral edema in DKA x4

Higher initial BUN Lower initial CO2 Low sodium Treatment with bicarbonate

How to monitor patients with DKA x4

Record and monitor fluid balance and lab results (initial and other ) Measure serum glucose every hour during treatment Assess neurological and mental status at frequent intervals Assess for cerebral edema if there’s headache or deterioration of mental status

Autoimmune diseases associated with DM x4

Hashimoto thyroiditis Type A gastritis Celiac disease Primary adrenal insufficiency