AH1 Flashcards
Red flags for pneumonia
RR>30 systolic BP<90 O2 sats less than 92 acute onset of confusion Heart rate >100 Multilobar involvement of the chest
COPD-X
Confirm the diagnosis Optimise function prevent deterioration develop a plan of care manage eXacerbations
What kind of rehabilitation is MUST with COPD
pulmonary rehabilitation- patient assessment, exercise training, education, behaviour change, nutritional intervention and psychosocial support
What co-morbid condition do we need to worry about in COPD
Osteoporosis- due to the medications and lack of activty and COPD presents in the elderly patient
Beck’s triad for cardiac tamponade
JVP distension
muffled heart sound
Hypotension
Carcinoid triad syndrome
Facial flushing
Diarrhea
Right-sided heart failure
Charcot’s triad of Multiple sclerosis
Nystagmus
Intention tremor
Scanning or staccato speech
Cushing’s triad for increased ICP
Hypertension(progressively increasing systolic pressure +/- widened pulse pressure)
Bradycardia
Irregular breathing
Mackler triad for Boerhaave syndrome
Rupture of the oesophagus during forceful emesis
- vomiting
- lower chest pain
- subcutaneous emphysema
Which test for supraspinatus tendinopathy
Hawkins Kennedy test
What are the tests for a supraspinatus tear
Drop Arm test and empty can test
What is the test for dislocation or anterior shoulder instability
Apprehension and relocation test
walking on heel is done by L
L5
Walking on toes is done by
S1
Which drugs give steven-johnson syndrome
Ethosuximide, Carbamazepine and lamotrigine
All patients with suspected TIA should have stroke risk assessment, which may include the ABCD2 tool
age>60 years
BP-140/90
Clinica features- unilateral weakness(2 points), speech impairment without weakness(1 point)
Duration >60 minutes(2 points), 10-59 minutes(1 min)
Diabetes- 1 point
Which 3 organs are most likely to be damaged by emboli
Brain
Kidney
Spleen
3 complications of long-standing AF
- Acute left heart failure → pulmonary edema
- Thromboembolic events: stroke/TIA, renal infarct, splenic infarct, intestinal ischemia, acute limb ischemia
- Life-threatening ventricular tachycardia
What are 4 ECG characteristics of AF
- Irregularly irregular RR intervals
- P-waves are indiscernible
- Tachycardia
- Narrow QRS complex (< 0.12 seconds)
State some investigations for AF you would like to do and why
- Troponin levels: to rule out myocardial infarction
- D-dimer levels: if risk factors (e.g., DVT) or clinical features of pulmonary embolism are present
- Brain-natriuretic peptide (BNP): to rule out heart failure
4.CBC: to identify anemia, infection - TSH, fT4: to screen for hyperthyroidism
6Serum electrolytes (Na+, K+, Mg2+, and Ca2+): to identify electrolyte imbalances - BUN, serum creatinine: to identify chronic kidney disease
- Ethanol levels, digoxin levels and/or urine toxicology (e.g., cocaine, amphetamines)
ECHO for imaging
What are the general principles of treating AF(3)
- Correcting reversible causes and/or treatable conditions (e.g., hyperthyroidism, electrolyte imbalances)
- Controlling heart rate and/or rhythm
- Providing anticoagulation
Controlling heart rate in AF
- what to do if they are stable
- what to do if they are unstable
Unstable AF: emergent electrical cardioversion
Stable AF: rate control or rhythm control strategies to control AF and prevent long-term recurrence
What are the rate control methods for AF
Normally good for the ELDERLY patient
1st choice: beta blockers (esmolol, propanolol, metoprolol) OR nondihydropyridine calcium channel blockers (diltiazem, verapamil)
2nd choice: digoxin
3rd choice: amiodarone
If not working albative procedures
What is a prerequisite for cardioversion in a patient in AF
Anticoagulation
New-onset AF (< 48 hours) in patients with:
-Tell me what you would do for low risk
-for high-risk patient
and what’s your medication choices
Low thromboembolic risk (see CHA2DS2-VASc score below) → consider anticoagulation directly before or after cardioversion
High thromboembolic risk → start anticoagulation immediately before or after cardioversion
Anticoagulation options: IV heparin or LMWH, direct thrombin inhibitors (e.g., dabigatran), or factor Xa inhibitors (e.g., rivaroxaban, apixaban)
AF ≥ 48 hours in patients with:
-Stable vs unstable
Unstable AF (require urgent cardioversion): IV heparin or LMWH immediately before cardioversion followed by warfarin for up to 4 weeks after cardioversion
TEE to rule out atrial thrombi recommended if anticoagulation has not been administered at least 3 week prior to cardioversion
Stable AF (do not require urgent cardioversion): warfarin with bridging therapy for 3 weeks before and up to 4 weeks after cardioversion
Anticoagulation therapy should be considered in all patients who are about to undergo cardioversion.
Write down CHA2DS2-VASc score for
-Non-valvular AF- like what is the treatment, what are the indications for each of these treatments(medications)
Nonvalvular atrial fibrillation: The need for anticoagulation therapy is based on the CHA2DS2-VASc score
Score = 0: no anticoagulation
Score = 1: no anticoagulation OR treatment with oral anticoagulants
Score ≥ 2: oral anticoagulation with either warfarin or newer oral anticoagulants (dabigatran, rivaroxaban, apixaban) - NOACs are avoided in patients with renal insufficiency
If warfarin is chosen then needed to monitor INR and has to be 2-3
Valvular AF and CHA2DS2-VASc score
Valvular atrial fibrillation: anticoagulation with warfarin is required regardless of the CHA2DS2-VASc score
The risk of stroke among patients with AF and mitral stenosis is 4 times greater than the risk of stroke with non-valvular stenosis.
A higher therapeutic range for INR of 2.5–3.5 is allowed. Dabigatran is not recommended among AF patients with a mechanical heart valve.
Acute management of AF
Mx dependant on Haemodynamic stability
- Haemodynamically unstable- Emergency electrical cardioversion
- Haemodynamically stable- Consider the risk of thromboembolism before cardioverting with either a drug or a direct current (DC) shock. Mx further dependent on duration of Afib (if in doubt mx as per >48 hours.
- AFib lasting less than 48 hours –> low risk of acute thromboembolic complications–> Consider initial rate/rhythm control stratergy. If using rhythm control, ensure anticoagulation (LWMH) at the time of electrical cardioversion and continued long term depending on thromboembolic risk.
- AFib lasting longer than 48 hours–> increased risk of developing a left atrial thrombus –> do not perform acute cardioversion unless left atrial thrombus has been excluded (using TOE, start anti-coag at time of cardioversion and continue for atleast 4 weeks), or the patient has had therapeutic anticoagulation for the previous 3 weeks. If not excluded/ no prior anti-coag- use rate control method.
Can I give antiplatelet therapy to reduce the risk of AF and reduce the risk of stroke from it
Recommendation: Antiplatelet therapy is not recommended for stroke prevention in Non-VAF patients, regardless of stroke risk.
1st choice drug for focal seizures
eTG states–> Carbamazepine(carbs are bad, that why you get rid of them first)
Lamotrigine–> cause he is a LAMO, that why he can only do focal control
and it causes SJS- cause its lame :P
1st choice of drug for generalized seizures
Valproate–> cause val means honour, they can do more
1st choice of drug for typical absence seizures
Ethosuximide
What is Todd’s paralysis and when does it occur
Occurs in focal seziures/simple partial seizures
Todd’s paralysis: Postictal weakness or paralysis of the affected limb or facial muscles (for minutes or up to hours)
What is the difference between simple partial and complex seizures- focal seizures
Focal seizure with intact consciousness (simple partial seizures)
Focal seizure with impaired consciousness (complex partial seizures)
What is an aura in seizures
Can get it tonic-clonic seizures-prodromal
A class of symptoms present in ∼ 25% of patients with migraines. Characterized by paroxysmal, reversible, focal neurologic symptoms that typically precede migraine headaches and last up to one hour. Symptoms may be visual (e.g., flashing lights), motor (e.g., paresis), somatosensory (e.g., paresthesia), vestibular (e.g., dizziness), or vocal (e.g., aphasia).
What is Adam-stokes attack
A sudden loss of consciousness, usually without warning and lasting for a few seconds, due to an abnormal heart rhythm (especially complete atrioventricular block).
What is the important factoid that can differentiate seizure from syncope
Postictal disorientation is key to differentiating between seizures and syncope. Syncope may be accompanied by twitches; however, patients become completely reoriented after a few seconds!
What is the biggest complication with status epilepticus
Status epilepticus is a life‑threatening event! If not interrupted, it can lead to cerebral edema, a dangerous rise in body temperature, rhabdomyolysis, and cerebral cardiovascular failure!(death)
Traveller’s diarrhea
Enterotoxigenic Escherichia coli (ETEC)
May be exudative-inflammatory diarrhea or secretory diarrhea
Erythromycin
Erythromycin promotes emptying of the stomach, improving visibility during gastroscopy.
What are the 2 types of gastritis and what are the clinical features
-investigations
AMAG(Autoimmune destruction of the parietal cells)
Associated with major histocompatibility haplotypes HLA-B8 and HLA-DR3
Associated with other autoimmune diseases (e.g., autoimmune thyroiditis)
Autoantibodies against intrinsic factor → vitamin B12 deficiency → pernicious anemia
EMAG(Environmental metaplastic atrophic gastritis) Helicobacter pylori infection (most important risk factor of atrophic gastritis overall) Dietary factors (e.g., N-nitroso compounds , alcohol intake, high salt intake)
Clinical features
Intensity of symptoms may be inconsistent and vary widely
Hematemesis (coffee-ground appearance or bright red in color), possibly melena
Epigastric pain is possible
Nausea, vomiting
Abdominal paresthesia and dyspepsia
IDA and Vitamin b12 deficiency
Ix
Vitamin B12 levels: decreased in AMAG
Serum gastrin levels: increased in AMAG
Serology : anti-intrinsic factor and anti-parietal cell antibodies
ALARMS symptoms of dyspepsia
ALARM Symptoms [mnemonic]
Anaemia (iron deficiency) Loss of weight Anorexia Recent onset of progressive symptoms Melaena/haematemesis Swallowing difficulty
If dyspepsia and either >55yrs or ALARM Symptoms then ENDOSCOPY
What is the empirical therapy for GERD
If GERD is clinically suspected and there are no indications for endoscopy, empiric therapy – ranging from lifestyle modifications to a short trial with PPIs – should be initiated. A GERD diagnosis is assumed in patients who respond to this therapeutic regimen.
What are some side effects of PPIs
Clostridium difficile infection
pneumonia
decreased serum vitamin B12 concentration (long-term use >2 years)
chronic kidney disease
fracture (long-term use); for patients at risk of osteoporosis and taking PPIs long term (>1 year), consider daily calcium intake and vitamin D status
Vitamin B12 deficiency and neurological damage- what are they
Patients with vitamin B12 deficiency present with signs of symmetrical damage to large sensory fibres
- decreased vibration sense
- decreased proprioception
- paresthesias
- hyporeflexia
What are the 2 main functions of Vitamin b12/cobalamin
- An essential role in enzymatic reactions responsible for red blood cell (RBC) formation
- Proper myelination of the nervous system
What is the main cause of vitamin b12 deficiency and state some others causes
Pernicious anemia: most common cause of vitamin B12 deficiency
Atrophic gastritis (e.g., secondary to H. pylori infection)
Gastrectomy
↓ Reduced uptake of IF-vitamin B12 complex in terminal ileum: e.g., Crohn’s disease, celiac disease, pancreatic insufficiency, surgical resection of the ileum
Other causes
Malnutrition: e.g., chronic alcoholism, anorexia nervosa, or strict vegan diets
What is the triad of condition to look out for if you have pernicious anaemia
Associated with other autoimmune diseases (e.g., hypothyroidism, vitiligo)
What is your ddx for polyneuropathies
Diabetic polyneuropathy- affects all kinds of nerve
Vitamin B12 deficiency-only large sensory fibres
Alcoholic polyneuropathy- Does not affect the autonomic fibers
Guillain-Barré syndrome
Exposure to lead, dapsone, amiodarone, or vincristine
Uremia
Vasculitis
Out of all the polyneuropathies, why does vitamin b12 have a positive Romberg’s test
Due to subacute combined degeneration of the spinal cord. Only affects the Large sensory fibers.
Vanish DDT- Cerebellar signs in the neuro exam
vertigo ataxia- during the gait, the patient will fall onto the side of the lesion nystagmus intention tremor staccato speech hypotonia dysmetria dysdiadochokinesia titubation.
Romberg’s test is a test of
proprioception
I say(Related to liver) you say
- pANCA
- anti-smooth antibodies
- Anti-mitochondrial antibodies (AMA)
PSC
Autoimmune hepatitis
PBC(affects women and women need a lot of energy-mitochondrial to do household and they are more introverted so they are only in the intrahepatic ducts)
What is the test used to check for albuminuria/proteinuria(mean the same thing cause the main protein peed out is albumin)
-what do you need to tell the patient
urinary albumin:creatinine ratio (urine ACR).
Need first void urine
If this is not possible, your doctor can still do the test on a sample of urine collected at any time during the day (called a spot random sample).
State the kidney function stage
1 ≥90 2 60-89 3a 45-59 3b 30-44 4 15-29 5 <15 or on dialysis
State the albuminuria stages and what is the unit
Normal
(urine ACR mg/mmol)
Male: < 2.5
Female: < 3.5
Microalbuminuria
(urine ACR mg/mmol)
Male: < 2.5 -25
Female: < 3.5-35
Macroalbuminuria
(urine ACR mg/mmol)
Male: > 25
Female: > 35
24 hour urine collection – the “gold standard”
Most patients with CKD are morelikely to DIE from CVD than get kidney failure
Proteinuria is not just a disease marker,
it influences disease progression
Mnemonic for indications for dialysis: A-E-I-O-U
Acidosis Electrolyte abnormalities (hyperkalemia) Ingestion (of toxins) Overload (fluid) Uremic symptoms
Metabolic acidosis of pH < 7.1
Hyperkalemia, hypercalcemia
Toxic substances (e.g., lithium, toxic alcohols)
Refractory fluid overload
Signs of uremia, including pericarditis, encephalopathy, and asterixis on exam
Complications of Nephrotic Syndrome(5)
- Edema
- Malnutrition
- Hypercoagulability
- Hyperlipidemia
- Increased risk of infection
What is included in the haemolytic screen
Common laboratory findings, such as elevated indirect bilirubin and lactate dehydrogenase, reticulocytosis, and decreased haptoglobin levels. The Coombs test helps to distinguish autoimmune (positive Coombs test) from non-autoimmune anemias (negative Coombs test).
Increased
- absolute reticulocyte count
- LDH (elevation is more pronounced in intravascular haemolysis)
- Indirect Bilirubin (i.e. unconjugated)
- Plasma free haemoglobin (PFHb)
Decreased
5. Haptoglobin (intravascular haemolysis)
Urine
Haemoglobin
Haemosiderin (useful in the diagnosis of intravascular haemolysis)
Blood film- look at spherocytosis, G6PD deficiency
Native valve endocarditis-Triple therapy
Gentamycin IV
Benzylpenicillin IV
Fluclocaxillin IV(MSSA better)
if MRSA–> change flucloxacillin to Vancomycin IV
Prosthetic valve endocarditis-Triple therapy
Gentamycin IV
Benzylpenicillin IV
Vancomycin IV
DDX for angina-4
- Anaemia
- Aortic stenosis
- Thyrotoxicosis
- Hypertrophic cardiomyopathy
Which heart failure does not show improvement with drugs
HFpEF–> Diastolic heart failure
What are some causes of heart failure
- Coronary artery disease, myocardial infarction
- Arterial hypertension
- Valvular heart disease
- Diabetes mellitus (diabetic cardiomyopathy)
- Renal disease
- Infiltrative diseases (e.g., hemochromatosis, amyloidosis)
What are some clinical features for heart failure-5
SOB Nocturia Fatigue Tachycardia Heart sounds--> S3/S4 Pulus alternans
What are the three main causes of heart failure
Hypertension
T2DM
CAD
Chronic compensated CHF definition
clinically compensated CHF; the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable
Acute decompensated CHF definition
Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction)
Why use CXR in heart failure
Useful diagnostic tool to evaluate a patient with dyspnea and differentiate CHF from pulmonary disease
State some lifestyle modification for heart failure patients
Salt restriction (< 3 g/day)
Fluid restriction in patients with edema and/or hyponatremia
Weight loss and exercise
Cessation of smoking and alcohol consumption
Immunization: pneumococcal vaccine and seasonal influenza vaccine
Contraindicated in acute decompensated heart failure!- which drug
Beta-blockers
Digoxin is contraindicated in HF when there is
Contraindicated in severe AV block
Which three drugs are contraindicated in HF
- NSAIDs
Worsen renal perfusion
Reduce the effect of diuretics
May trigger acute cardiac decompensation - Calcium channel blockers (verapamil and diltiazem): negative inotropic effect; worsen symptoms and prognosis
- Thiazolidinediones: promote the progression of CHF (↑ fluid retention and edema) and increase the hospitalization rate
4 ddx for pericarditis
- ACS
- Myocarditis
- PE
- Pericarditis fluid accumulation–> Beck’s triad–> muffled sounds, JVP distension and hypotension
What are 2 invasive procedures for heart failure
Implantable cardiac defibrillator (ICD): prevents sudden cardiac death
Primary prophylaxis indications
CHF with EF < 35% and prior myocardial infarction/CHD
Increased risk of life-threatening cardiac arrhythmias
Secondary prophylaxis indications: the history of sudden cardiac arrest, ventricular flutter, or ventricular fibrillation
Cardiac resynchronization therapy (biventricular pacemaker): improves cardiac function
Indications: CHF with EF < 35%, dilated cardiomyopathy, and left bundle branch block
Can be combined with an ICD
Device Therapy
- ICD (Internal cardac debrillator)
Primary pevention, EF < 30-25%
Secondary-Hx of sustained ventricular arrythmias or sudden cardiac death
- Cardiac Resynchronization
Used in patients w/ a conduction delay, meaning ventricle contract at different times.
This foorces all walls of the heart to contract at the same time
- QRS 140
- EF < 35%
- NYHA 11-1V
- Optimal medical treatment
What are some causes for Acute decompensated heart failure
Cardiac decompensation is the most common reason for hospital admissions and is the most important complication of congestive heart failure.
Exacerbation of congestive heart failure (e.g., through pneumonia, anemia, volume overload, medication noncompliance)
Acute myocardial infarction
Atrial fibrillation, severe bradycardia, and other arrhythmias
Myocarditis
Hypertensive crisis
Pulmonary embolism
Pericardial tamponade
Aortic dissection
Cardiotoxic substances
Renal failure
Cardiodepressant medication (e.g., beta blockers, CCBs)
Management of ADHF can be remembered with “LMNOP”:
: L = Lasix (furosemide), M = Morphine, N = Nitrates, O= Oxygen, P = Position (with elevated upper body).
Hemodynamic stabilization: inotropes (e.g., dobutamine) in case of systolic dysfunction
Benzo and delirium? What should we do?
Benzodiazepines are deliriogenic. Do not treat delirious patients with benzodiazepines unless the delirium is due to alcohol or benzodiazepine withdrawal, in which case haloperidol is contraindicated because it lowers the seizure threshold!
Alternative: atypical antipsychotics (e.g., olanzapine)
What is the treatment for acute pericarditis and constrictive pericarditis
Often self-limiting and resolves within approximately 2-6 weeks–>
- treat the underlying cause
- Restricted physical activity
- NSAIDs + colchicine(alleviate symptoms, reduce the rate of recurrence)
Constrictive–> treat the underlying the cause, symptomatic therapy and pericardiectomy
Complications–>
1) constrictive pericarditis
2) cardiac tamponade
Pink frothy sputum
Pulmonary edema
Acute cardiogenic pulmonary edema
-what are the common symptoms
It is a medical emergency dyspnea cough pink frothy sputum anxiety chest pain
Acute pulmonary edema- CXR what do you see
ABCDE of heart failure
Neuropathic arthropathy in T2D, another name is
Charcot joints
What are the common findings on Ix shared by haemolysis
elevated indirect bilirubin and lactate dehydrogenase, reticulocytosis, and decreased haptoglobin levels.
What is Coomb’s test used to detect
The autoimmune (positive Coombs test) Non-autoimmune anemias (negative Coombs test).
What is the difference between intravascular and extravascular haemolysis
intra-vascular haemolysis occurs inside the blood vessels
extra-vascular haemolysis occurs in other parts of the body (e.g. spleen)
causes may overlap and haemoglobin from extravascular haemolysis may still enter the circulation
What are some causes of cold autoimmune haemolysis
Etiology: mostly IgM antibodies (bound to erythrocytes) that can cause both intravascular and extravascular hemolysis
Primary
Idiopathic (esp. in the elderly)
Secondary
Mycoplasma or EBV infection
Malignancy (e.g. non-Hodgkin lymphoma, chronic lymphocytic leukemia)
Heinz bodies
oxidative stress in G6PD deficiency
liver disease
thalassemia
splenectomy
2 surgical procedures for hernia repair
Open vs lap
Surgical mesh repair (hernioplasty)
Surgical hernia repair (herniorrhaphy)
What is Courvoisier sign
Enlarged gallbladder and painless jaundice
Painless jaundice (a nontender gallbladder) is the most common initial symptom of pancreatic cancer but usually doesn’t occur when the primary tumor is located in the tail or body of the pancreas.
This will only happen if its the head
What is the main cause of HCC
State some other causes of HCC
Liver cirrhosis
Chronic hepatitis B or C virus infection Nonalcoholic steatohepatitis (NASH) Hemochromatosis Wilson's disease Alpha-1 antitrypsin deficiency Alfatoxins
HCC blood test is
AFP
Mirizzi syndrome
Gallstones in the cystic duct or Hartmann pouch of the gallbladder obstruct the common hepatic duct or common bile duct.
Symptoms resemble those of choledocholithiasis.
Can also lead to cholecystocholedochal fistula
Wernicke’s aphasia
Receptive problem/cannot understand words others are saying, hence its alot WORK(W for W–> Wernicke’s)
Receptive
Inability to understand words(alot of words)
Can speak fine, but does not respond properly to questioned being asked
Broca’s aphasia
Non-fluent aphasia
Expressive aphasia
Cannot find words
BEE are unable to say
DKA in adults- what should the ketones been
0.6 -1.5 - moderate risk of DKA
greater than 1.5 definitely suspicious of DKA-High risk
Criteria for DKA in adults
DKA = pH<7.35
HCO3<15
and mAG and ketones>1.
BGL may be normal or elevated–> CAN BE NORMAL
Which patients are a higher risk of cerebral oedema in DKA
Young patients
Cerebral oedema, what actions must be taken
How to take action:
• Monitoring for signs of cerebral oedema should start
from the time of admission and continue up to at least
24 hours after admission
• If there is suspicion of cerebral oedema or the patient
is not improving within 4 hours of admission, call the
consultant
• Undertake CT scan to confi rm fi ndings
• Consider ICU (an indication for checking arterial blood
gases)
• Consider IV mannitol (100mL of 20% over 20 minutes)
or dexamethasone 8mg (b
What is the Osmolality calculation
Osmolality = 2 x (serum sodium + serum potassium) + glucose + urea
What is the screening, diagnostic test and monitoring celiac disease(according to eTG)
Screening-
IgA (anti‑)tissue transglutaminase antibody (tTG), IgG anti-deamidated gliadin antibody, also always do total IgA because of potentially associated IgA deficiency.
Diagnosis- Duodenal biopsy- showing intra epithelial lymphocytes and villis blunting/atrophy
Monitoring- Repeat anti-body testing, can take 12 months for Ab levels to normalise, intestinal healing can take up to two years, therefore, repeat duodenal biopsy should now be performed following at least 12 months of gluten-free diet
What are some clinical consequences of decompensated cirrhosis
Portal hypertension Ascites Hepatic encephalopathy Coagulopathy Hepatorenal syndrome
Features of cardiac hemochromatosis
1) Cardiomyopathy (restrictive or dilated)
2) Cardiac arrhythmias: paroxysmal atrial fibrillation (most common), sinus node dysfunction, complete AV block, atrial and ventricular tachyarrythmias, and sudden cardiac death
3) Congestive heart failure
In combination with diabetes mellitus, bronze-coloured skin pigmentation is also referred to as “bronze diabetes.”
Cerebral ring enhancing lesions (mnemonic)
DR MAGIC
M: metastasis
A: abscess
G: glioblastoma
I: infarct (subacute phase), inflammatory - neurocysticercosis (NCC), tuberculoma
C: contusion
D: demyelinating disease (the classically incomplete rim of enhancement)
R: radiation necrosis or resolving hematoma
What are the common causes-3 of cirrhosis
Alcoholic liver disease, Hepatitis C, and NASH are the most common causes of cirrhosis
List out of conditions which can cause cirrhosis
Hepatotoxicity
Long-standing alcohol abuse (one of the two most common causes of chronic liver disease in the USA)
acetaminophen
Ingesting aflatoxin created by Aspergillus
Inflammation (Chronic) viral hepatitis B, C, and D ; Chronic hepatitis C is now the most common cause of cirrhosis in the US Primary biliary cirrhosis Primary sclerosing cholangitis Autoimmune hepatitis
Metabolic disorders Non-alcoholic steatohepatitis Hemochromatosis Wilson's disease Alpha‑1 antitrypsin deficiency Hepatic vein congestion or vascular anomalies Budd-Chiari syndrome
What classification is used for cirrhosis severity classification
Child-Pugh score
What is the treatment for ascites(eTG)
1st Spironolactone, add frusemide if spironolactone alone is inadequate
Spironolactone and furosemide to manage ascites and edema in patients with hypoalbuminemia
What are intervention procedures that can be done for cirrhosis
TIPS (transjugular intrahepatic portosystemic shunt) to lower portal pressure
Surgery: A liver transplant is the only curative option in advanced liver disease.
List out some complications of cirrhosis
Portal hypertension Hepatic encephalopathy Hepatorenal syndrome Portal vein thrombosis Pulmonary complications of portal hypertension
Hepatic encephalopathy
-clinical manifestation
Hepatic encephalopathy (HE) is defined as fluctuations in mental status and cognitive function in the presence of severe liver disease.
- Disturbances of consciousness, ranging from mild confusion to coma
- Multiple neurological and psychiatric disturbances like:
1) Asterixis
2) Memory loss
3) Disoriented, socially aberrant behaviour
4) Muscle rigidity
Elevated ammonia
Treatment of encephalopathy
Lactulose: synthetic disaccharide laxative
First-line treatment for HE
What is the treatment of choice for diabetes inspidius(centra)
Desmopressin, a synthetic ADH analog, is the treatment of choice in central DI.
Which form of diabetes inspidius is more common
Central
nephrogenic is rare
DI- what test can confirm it
Water deprivation test
Which drugs cause hyperprolactinemia
Dopamine antagonists:
Antiemetics: metoclopramide
Antipsychotics (e.g., haloperidol, risperidone)
What are 2 causes of physiological hyperprolactinemia
Pregnancy and lactation
What chemical in the brain inhibit prolactin
Dopamine
What is the treatment of choice for hyperprolactinemia
Dopamine agonists (treatment of choice): bromocriptine, cabergoline
“CUSHINGOID” is the acronym for side effects of corticosteroids:
C = Cataracts U = Ulcers S = Striae/Skin thinning H = Hypertension/Hirsutism/Hyperglycemia I = Infections N = Necrosis (of femoral head) G = Glucose elevation O = Osteoporosis/Obesity I = Immunosuppression D = Depression/Diabetes
State cause clinical features of Cushing’s syndrome
Skin Thin, easily bruisable skin with stretch marks (classically purple abdominal striae) and/or ecchymoses Flushing of the face Hirsutism Acne
Neuropsychological: lethargy, depression, sleep disturbance, psychosis
Musculoskeletal
Osteopenia; osteoporosis; pathological fractures; avascular necrosis of the femoral head
Muscle atrophy/weakness
What is the most common clinical feature seen by Cushing’s syndrome
Secondary hypertension
Which hormone is high in Cushing’s
Cortisol
Conn syndrome is
Primary hyperaldosteronism
It is typically due to adrenal hyperplasia or adrenal adenoma.
What is the most common clinical feature of Conn syndrome
Primary hyperaldosteronism is one of the common causes of secondary hypertension.
Drug treatment HTN
What is the confirmatory test and best initial test for phaeochromocytoma
Best initial test: metanephrines in plasma (high sensitivity)
Confirmatory test: metanephrines and catecholamines in 24-hour urine(high specificity)
CAH one disease or many
Many
All forms of CAH are characterized by low levels of cortisol, high levels of ACTH, and adrenal hyperplasia.
What is the most common cause of CAH and what do you see in those kinds of patients
The most common form of CAH, which is caused by a deficiency of 21β-hydroxylase, presents with
1) hypotension
2) ambiguous genitalia
3) and virilization (in the female genotype)
4) and/or precocious puberty (in both males and females
What is Addison’s disease
Primary adrenal insufficiency
What is the difference between secondary and tertiary Addison’s disease
Secondary adrenal insufficiency is the result of decreased production of ACTH (adrenocorticotropic hormone) and tertiary adrenal insufficiency is the result of decreased production of CRH (corticotropin-releasing hormone) by the hypothalamus.
What is adrenal haemorrhage
Waterhouse‑Friderichsen syndrome
The most common cause of Addison’s disease is
Autoimmune adrenalitis
Out of the 1,2,3 adrenal insufficiency
Secondary and tertiary adrenal insufficiency are far more common than primary adrenal insufficiency!
Primary adrenal insufficiency Pigments the skin. Secondary adrenal insufficiency Spares the skin. Tertiary adrenal insufficiency is due to Treatment (cortisol).
PP
SS
TT
Just a mnemonic-know it I guess
What are the electrolyte disturbances in Addison’s disease
Hyponatremia
Hyperkalemia
Normal anion gap metabolic acidosis
Hypoglycemia
Blood test for Addison’s
Morning serum cortisol
ACTH stimulation test
Treatment for adrenal insufficiency
Glucocorticoid replacement therapy with hydrocortisone is required in all forms of adrenal insufficiency!
Adrenal crisis
- causes
- clinical features
1) Stress (e.g., infection, trauma, surgery) in a patient with underlying adrenal insufficiency
2) Sudden discontinuation of glucocorticoids after prolonged glucocorticoid therapy
clinical features
1) Hypotension, shock
2) Impaired consciousness
3) Fever
4) Vomiting, diarrhea
5) Severe abdominal pain (which resembles peritonitis)
6) Hypoglycemia, hyponatremia, hyperkalemia, and metabolic acidosis
The 5 S’s of adrenal crisis treatment are
Salt: 0.9% saline, Sugar: 50% dextrose, Steroids: 100 mg hydrocortisone IV every 8 hours, Support: normal saline to correct hypotension and electrolyte abnormalities, Search for the underlying disorder
Adrenal crisis can be life-threatening. Therefore, treatment with high doses of hydrocortisone should be started immediately without waiting for diagnostic confirmation of hypocortisolism!
Which hyperglycemia state/emergency will present with more volume depletion
HHS
HHS patients, in contrast to those with DKA, will present with more extreme volume depletion
What are 3 clinical features in DKA you don’t see in HHS
Signs and symptoms specific to DK
1) Rapid onset (< 24 h) in contrast to HHS
2) Abdominal pain
3) Fruity odour on the breath; from exhaled acetone
4) Hyperventilation: Kussmaul respirations: deep breaths at a normal respiratory rate
DKA is quite insidious however HHS is developed over days
Why is there hypovolemia in DKA
Insulin deficiency → hyperglycemia → hyperosmolality → osmotic diuresis and loss of electrolytes → hypovolemia
DKA criteria in eTG
DKA - eTg
- ph <7.3
- Serum bicarbonate <15 mmol/l
- Aniom gap >12 mmol/l
- Elevated blood ketone/positive urine ketone
- Blood glucose > 14 mmol/l/ Can be normal too
Treatment of DKA
Treat DKA with normal saline and regular insulin.
Fluid replacement (and regular monitoring of volume status)
Isotonic saline solution (0.9% sodium chloride)
Insulin (and hourly serum glucose monitoring until stable)
low-dose insulin therapy with IV regular insulin
What is the treatment of HHS
HSS Managment eTg
1. Aggressive fluid replacement with 0.9% sodium chloride- Isotonic saline
- Insulin only if BSL stops dropping after fluid replacement(if hyperglycemia is still NOT settled down, then you give Insulin)
- Potassium replacement is independent of patient circumstance
- HSS patients are at a very high risk of arterial and venous thrombosis, therefore use anti-coagulant prophylaxis.
What prophylaxis needs to be given in HHS patients
HSS patients are at a very high risk of arterial and venous thrombosis, therefore use anti-coagulant prophylaxis.
State 2 complications of hyperglycemia emergencies
Cerebral edema and cardiac arrhythmias
Which two complications of hypothyroidism are fatal
Myxedema coma and myxedematous heart disease
State 2 common drugs that cause hypothyroidism as a side effect
Lithium and amiodarone
The most common cause of hypothyroidism in iodine-rich nation
Hashimoto thyroiditis
Abnormal menstrual cycle (esp. secondary amenorrhea or menorrhagia)
–> why in hypothyroidism and state similar symptoms because of this cause
Hyperprolactinemia: prolactin production is stimulated by TRH → increased prolactin suppresses LH, FSH, GnRH, and testosterone secretion; also stimulates breast tissue growth
Symptoms of hyperprolactinemia–>
Abnormal menstrual cycle (esp. secondary amenorrhea or menorrhagia)
Galactorrhea
Decreased libido, erectile dysfunction, delayed ejaculation, and infertility in men
Which thyroiditis painful
Subacute granulomatous thyroiditis (De Quervain)
DDx for hypothyroidism
Hashimoto thyroiditis
Postpartum thyroiditis
Subacute granulomatous thyroiditis (De Quervain) Congenital hypothyroidism
Riedel thyroiditis
Which antibodies are detected against autoimmune hypothyroidism
Tg Ab (thyroglobulin) and TPO Ab (thyroid peroxidase): detectable in most patients with autoimmune hypothyroidism
Tell me a obstetric cause of hyperthyroidism
Gestational trophoblastic disease(GTD)
β-hCG-mediated hyperthyroidism (hydatidiform mole, choriocarcinoma)
High levels of beta-HCG mimic thyroid hormone so yeah
DDX for hyperthyroidism
Neuropsychiatric symptoms: anxiety/panic disorders
Hyperadrenergic symptoms: intoxication with anticholinergics; cocaine/amphetamine abuse; withdrawal syndromes
Weight loss: diabetes mellitus, malignancy
Cardiac symptoms: congestive cardiac failure
Graves disease
Toxic multinodular goitre
Subacute granulomatous thyroiditis (de Quervain thyroiditis)
Subacute lymphocytic thyroiditis (silent thyroiditis)
Iodine-induced hyperthyroidism
Exogenous hyperthyroidism or factitious hyperthyroidism
Symptomatic therapy of thyrotoxicosis
Beta-blockers provide immediate control of symptoms.
There are currently three effective initial treatment options for Graves disease
Antithyroid drugs
Radioactive iodine ablation
surgery.
Hyperthyroidism-pre-op consultation what is an important thing to state
and then post-op
Antithyroid drugs and beta-blockers are given preoperatively for at least 4–8 weeks–> To reduce the intraoperative risk of thyroid storm
Postprocedural care
Management of calcium levels: measurement of serum calcium and intact parathyroid hormone levels
Weaning of beta-blockers
How to prevent thyroid storm prior to surgery
Pretreatment with beta-blockers, antithyroid drugs, and potassium iodide has drastically decreased the incidence of thyroid storm in patients undergoing surgery.
Hyperthyroidism in pregnancy
-pathophysiology
Hyperthyroidism is rare in pregnancy (< 0.5% of cases).
Etiology: Graves disease and β-hCG-mediated hyperthyroidism are the most common causes.
β-hCG molecule has a similar structure to that of the TSH molecule.
β-hCG binds to TSH receptors of the thyroid gland → thyroid stimulation → hyperthyroidism
If hyperthyroidism during pregnancy, what should you suspect
Suspect a molar pregnancy or choriocarcinoma if severe hyperthyroidism manifests during pregnancy!
TSH receptor antibodies (TRAb) present
Graves disease
Thyroid peroxidase antibodies (TPOAb) present in
Hashimoto’s thyroiditis
Thyroglobulin antibodies (TgAb)
Hashimoto’s thyroiditis
Primary hyperparathyroidism-clinical features-there is a mnemonic
“Stones, bones, abdominal groans, thrones, and psychiatric overtones!”
stones-Nephrolithiasis, nephrocalcinosis
bones-Bone, muscle, and joint pain
abdominal groans–> gastric ulcers
thrones- constipation
psychiatric overtones-depression, fatigue, anxiety, sleep disorders
The most common cause of hypoparathyroidism
Postoperative: (most common cause of hypoparathyroidism in adults): secondary to thyroidectomy, parathyroidectomy, or radical neck dissection
second-most common-autoimmune
Chvostek sign
hypocalcemia → hyperexcitable nerves → tapping the facial nerve on the cheek → contraction of facial muscles
Trousseau sign
inflate BP cuff → allow for occlusion of brachial artery for a few minutes → carpal spasm
MEN 1: 3 “P”s
Parathyroid, Pancreas, Pituitary gland
MEN 2A: 1 “M”, 2 “P”s
Medullary thyroid carcinoma, Pheochromocytoma, Parathyroid
MEN 2B: 2 “M”s, 1 “P”
Medullary thyroid carcinoma, Marfanoid habitus/Multiple neuromas, Pheochromocytoma
DUMBBELLS
Used for cholinergic overdose
Diarrhoea. Urination. Miosis/muscle weakness. Bronchorrhea. Bradycardia. Emesis. Lacrimation. Salivation/sweating.
Anticholinergic mnemonic
Blind as a bat (mydriasis)
mad as a hatter (delirium)
red as a beet (flushing)
hot as a hare (hyperthermia)
dry as a bone (decreased secretions and dry skin)
the bowel and bladder lose their tone (urinary retention and paralytic ileus)
and the heart runs alone (tachycardia).”
Triad of septic arthritis
The classical triad of fever, joint pain, and restricted range of motion
Gonococcal arthritis
Gonococcal arthritis is the most common form of arthritis in sexually active young adults! In a young, sexually active adult presenting with classic symptoms of septic arthritis, the gonococcal infection must be ruled out!
Further management for arthritis
Tailor antibiotics to gram stain, culture and susceptibility results when available (see table below)
Continue antibiotic therapy at least ≥ 2 weeks
Continue serial drainage as needed
Immobilization + NSAIDs for pain relief and to reduce inflammation
Follow-up: Physiotherapy should be initiated early to prevent contracture of both the joint and its capsule
Most common complaint of Granulomatosis with polyangiitis
Upper respiratory manifestations (i.e., purulent, sometimes bloody discharge; chronic nasopharyngeal infections; saddle nose deformity) are the most common chief complaints!
Triad for Granulomatosis with polyangiitis
GPA triad: necrotizing vasculitis of small arteries, upper/lower respiratory tract manifestations, and glomerulonephritis!
Define shock
What are the types of shock
Shock is a life-threatening circulatory disorder that leads to tissue hypoxia and a disturbance in microcirculation.
The causes for inadequate organ perfusion may differ, but they all ultimately result in tissue hypoxia:
Loss of intravascular fluid → hypovolemic shock
Inability of the heart to circulate blood → cardiogenic shock
Redistribution of body fluid → distributive shock
Haemorrhagic shock is a
-what is it divided into
Hypovolemic shock
Hemorrhagic fluid loss and non-Hemorrhagic fluid loss
Cardiogenic shock is divided into
Non-obstructive cardiogenic shock
Obstructive cardiogenic shock
Cardiogenic shock with pulmonary edema, should you administer fluids for resus
Unlike other causes of shock the administration of intravenous fluids in most cases of cardiogenic shock would worsen cardiogenic pulmonary edema!
Types of distributive shock
Septic shock (most common)
Neurogenic shock
Anaphylactic shock
