Internal medicine Flashcards
(125 cards)
20.1 Cardiovascular effects of hyperthyroidism include
a) decreased diastolic relaxation
b) decreased SVR
c) decreased PVR
d) increased diastolic BP
Decreased SVR
- increased CO, increased SBP and decreased DBP with widened PP
Up to Date
Cardiovascular - Patients with hyperthyroidism have an increase in cardiac output, due both to increased peripheral oxygen needs and increased cardiac contractility. Heart rate is increased, pulse pressure is widened, and peripheral vascular resistance is decreased
23.1 During standard diagnostic nocturnal polysomnography for investigation of obstructive sleep apnoea, apnoea is defined as cessation of airflow for
A. 10 sec
B. 20 sec
C. 30 sec
D. 10 sec with 3% desat
E. 20 sec with 3 % desat
A
Apnea is defined as the cessation of airflow for ten or more seconds.
Hypopnea is defined as a recognizable, transient reduction, but not a complete cessation of, breathing for ten or more seconds.
Hypopnea requires a 4% fall in SpO2
https://www.ncbi.nlm.nih.gov/books/NBK441909/#:~:text=Obstructive%20Sleep%20Apnea%20(OSA)%2C,for%20ten%20or%20more%20seconds.
20.1 A 64-year-old man presenting for elective surgery is on thyroxine 100 mcg daily. His thyroid function tests are: (Thyroid function tests shown). These results are most consistent with
TFTs thryoxine TSH < .05 T4 and T3 completely normal
a) Hypophysectomy
b) Subclinical Hyperthyoirdism
c) Sick euthyroid
d) Toxic Multinodular goitre
b) Subclinical Hyperthyoirdism
Subclinical hyperthyroidism: low TSH, normal T3 + T4
Clinical hyperthyroidism: low TSH, high T3, high/normal T4
Subclinical hypothyroidism: high TSH, normal T3 + T4
Clinical hypothyroidism: high TSH, low/normal T3, i T4
Amiodarone: high/normal TSH, low T3 (2o to inhibition of pituitary T4 to T3 conversion)
Sick euthyroid: low TSH, low T3
Hypophysectomy (central hypothyroidism): low/normal TSH/T3/T4
Compliant on thyroxine: normal TSH, high/normal T3, low T4
Non-compliant w thyroxine (pt taking several tabs prior to Dr’s appointment): high TSH, normal T4
21.2 Of the following drugs, the least likely to cause pulmonary vasodilation when used at low
doses in patients with chronic pulmonary hypertension is
a) Dopamine
b) Dobutamine
c) Vasopressin
d) Milrinone
dopamine
- least likely to cause pulmonary vasodilation (all the others do to my knowledge)
- From UP TO DATE:
> At low doses of 1 to 3 mcg/kg per min, dopamine acts primarily on dopamine-1 receptors to dilate the renal and mesenteric artery beds
> At 3 to 10 mcg/kg per min (and perhaps also at lower doses), dopamine also stimulates beta-1 adrenergic receptors and increases cardiac output, predominantly by increasing stroke volume with variable effects on heart rate.
> At medium-to-high doses, dopamine also stimulates alpha-adrenergic receptors, although a small study suggested that renal arterial vasodilation and improvement in cardiac output may persist as the dopamine dose is titrated up to 10 mcg/kg per min
*clinically, the haemodynamic effects of dopamine demonstrate individual variability
Dobutamine (inodilator):
- selective β1-agonist that increases cardiac contractility and reduces pulmonary vascular and systemic vascular resistances
Vasopressin:
- vasopressin may have pulmonary vasodilatory effects in addition to a systemic vasoconstrictive effect
Milrinone (inodilator):
- the phosphodiesterase-3 inhibitors, milrinone and enxoimone, have positive inotropic effects combined with the capacity to reduce RV afterload (‘inodilators’) without significant chronotropic effect, but they can be associated with significant systemic hypotension
23.1 In patients with primary adrenal insufficiency, a markedly elevated renin is most likely due to
A Insufficient corticosteroid replacement
B Insufficient fludrocortisone replacement
C Excessive corticosteroid replacement
D Excessive fludrocortisone replacement
b. Insufficient fludrocortisone replacement
In Primary Adrenal Insufficency, cortisol deficiency results in decreased feedback to the HPA axis, leading to increased secretion of ACTH to stimulate the adrenal cortex. Simultaneously, MCs deficiency causes increased release of renin by the juxtaglomerular apparatus of the kidneys.
22.1 A 30-year-old parturient presents in labour. She has a history of Addison’s disease from autoimmune adrenalitis and has been taking prednisolone 6 mg daily for ten years. On presentation the patient is given hydrocortisone 100 mg intravenously. The most appropriate steroid replacement regimen the patient should receive during labour is
a. 25mg TDS hydrocortisone
b. 8mg/hr hydrocortisone
c. 6mg PO prednisone
8mg/hr
Guidelines for mx of glucocorticoids during the perioperative period for patients with adrenal insufficiency
https://associationofanaesthetists-publications.onlinelibrary.wiley.com/doi/10.1111/anae.14963
21.1 A 45-year-old man has the following results on his blood biochemistry testing (Liver function tests shown). The most likely diagnosis is
a. Cholecystitis
b. Metastatic liver disease
c. Hepatitis C
d. Chronic liver disease
e. Paracetamol toxicity
a. Cholecystitis
Example and explanation taken from RACGP:
The raised AlP relative to Alt suggests cholestasis and the high GGt confirms liver origin. The mild hyperbilirubinaemia confirms the clinical impression of jaundice. Biliary disease is highly likely with gallstones the most likely differential diagnosis. however, this clinical picture may also occur in drug reactions or infiltrative conditions. After a careful history, abdominal ultrasound is the most appropriate next investigation.
22.1 Complications of severe anorexia nervosa (body weight < 40% ideal) include all of the following EXCEPT
a. HypoK
b. Cl abnormality
c. Delayed gastric emptying
d. Hypercalcaemia
e. Cardiomyopathy
Hypercalcaemia
22.1 A 45-year-old man presents on the day of surgery for an elective inguinal hernia repair. He is well
but is noted to be mildly jaundiced. He takes simvastatin for hyperlipidaemia and has no other medical history. He consumes about three standard drinks of alcohol per day and does not smoke. He briefly experimented with illicit drugs more than ten years ago. His laboratory results show: (supplied) The most likely diagnosis is
Normal electrolytes
ALP 85 N
ALT 31 N
AST 31 N
GGT 15 N
Urea 10 [4-9]
Creatinine 103 N
Total protein 74 N
Albumin 40 N
BSL 4.2 N
Bilirubin 29 [0-20]
Conjugated 5
Unconjugated 24
A. Fatty liver
B. Hepatitis
C. Cholestasis
D. Gilbert syndrome
E. Drug induced
Gilberts
Gilbert’s syndrome is a benign genetic condition that commonly presents as incidental
hyperbilirubinaemia or painless jaundice.
It is relatively common with a population frequency of approximately 2–10%.
Gilbert’s syndrome is caused by defective bilirubin clearance by the hepatic conjugating enzyme UDP-glucuronosyltransferase
https://www.rcpa.edu.au/getattachment/8b9a8acf-f7f5-4088-951c-3f65f0c2f8fe/Interpreting-liver-function-tests.aspx
21.2 The condition in which volatile anaesthesia is least appropriate is
a) Multiple sclerosis
b) Myasthenia gravis
c) Lambert-Eaton syndrome
d) Guillain-Barre syndrome
e) Muscular dystrophy
e) Muscular dystrophy
- rhabdomyolysis risk if given to patients with Duchenne or Becker’s muscular dystrophy
- volatiles safe in all above, and also safe in patient’s with myotonic dystrophy
Malignant hyperthermia
- high mortality uncoupling regulation of RyR1 to SR
Duschenne muscular dystrophy
- fatal rhabdo (hyperkalaemia)
21.2 An electrocardiogram (ECG) abnormality which is NOT usually associated with severe anorexia nervosa is
a) Sinus tachycardia
b) Wandering atrial pacemakers
c) ST depression
d) T wave inversion
e) Prolonged QT
a) Sinus tachycardia
BJA: Anorexia nervosa: perioperative implications
https://academic.oup.com/bjaed/article/9/2/61/299563
Cardiovascular
Typically anorexic patients are hypotensive and bradycardic. These physiological markers may be used as indications for hospitalization.
Bradycardia reflects the decrease in basal metabolic rate that arises as an adaptive response to starvation. Although patients are usually in sinus rhythm, electrocardiographic abnormalities are common and may be found in >80% of strict dieters. These include: atrioventricular block, ST depression, T wave inversion, and QT prolongation.
QT prolongation may be caused by hypocalcaemia, hypomagnesaemia, drugs, or directly by starvation itself. Electrolyte disturbances have a significant causal role in ECG abnormalities.
Other factors, for example, atypical antipsychotics, may also contribute.
Associated arrhythmias include: sinus arrest, wandering atrial pacemakers, nodal escape beats, supraventricular tachycardia, and ventricular tachycardia.
The reported incidence of arrhythmias under anaesthesia is 16–62%.
With respect to myocardial contractility, left ventricular function has been demonstrated to be impaired in a proportion of patients. Echocardiographic studies have also demonstrated a higher incidence of mitral valve prolapse in anorexic patients. The reasons for this are not entirely clear. It is postulated that the loss of left ventricular volume and mass leads to abnormal mitral valve motion.
In addition to starvation-induced myocardial impairment, the myocardium may be specifically damaged by pharmacological agents.
For example, emetogenic ipecac syrup is directly cardiomyotoxic and produces inflammatory changes and myocardial fibre degeneration when used long term.
Rarely, antipsychotic drugs, for example, olanzapine, may cause cardiomyopathy.
Myocardial impairment can be caused by hypophosphataemia which also reduces the threshold for arrhythmias.
Compromised myocardial function requires judicious use of fluids perioperatively as there is an increased risk of congestive cardiac failure. Echocardiography along with invasive perioperative monitoring (central venous catheter) should be considered to prevent fluid overload.
During a routine preoperative examination of a patient’s heart, you note exaggerated splitting of the second heart sound with inspiration. This is characteristically heard in
A. Aortic Reguritation
B. HOCM
C. Left bundle branch block
D. Mitral Stenosis
E. Pulmonary Stenosis
E. Pulmonary Stenosis
DERANGED PHYSIOLOGY:
Splitting of the first heart sound
Right bundle branch block can produce a split first heart sound - because the contraction of the right ventricle is delayed- the conduction occurs via the left ventricle rather than the bundle of His- and thefore the closure of the tricuspid valve occurs after a substantial delay.
Atrial septal defect can result in a fixed split of the first heart sound
Splitting of the second heart sound
It is normal for this sound to be split. The high pressure in the systemic circulation slams the aortic valve shut rather abruptly, almost angrily. In contrast, low pressure of the pulmonary circulation tends to close the pulmonary valve gently, and therefore the pulmonary component of the second heart sound (P2) is usually delayed by about 20-30 milliseconds.
It is also normal for increased right ventricular filling to cause a widening of the split. The more blood in the RV, the longer it takes to eject, and therefore the greater the delay until pulmonary valve closure.
n the spontaneously breathing patient, the delay is greatest during inspiration. Naturally, in the patient ventilated with positive pressure the delay is greatest during expiration (positive pressure being a barrier to diastolic filling).
Increased normal splitting of S2
Anything that delays the end of right ventricular systole can cause this sort of picture.
Right bundle branch block - the delay in conduction via the left ventricle causes a delay in right ventricular contraction, and therefore a delay in pulmonary valve closure. The S1 will also be split.
Ventricular septal defect - because the right ventricle receives a large volume load directly from the left ventricle, and therefore takes longer to complete its systolic contraction.
Pulmonary valve stenosis - because the right ventricle takes longer to empty though a narrowed valve
Mitral regurgitation- not because right ventricular contraction is delayed, but because left ventricular contraction is shortened (as the LV empties in both the aortic and the atrial directuion, systole is over very quickly).
Fixed splitting of S2
Atrial septal defect - the atria, joined by a gaping hole in their seput, act as one atrium. The result is a reasonably equal distribution in volume betweent the right and left atrium. This way, both sides of the circulation share the same diastolic filling pressure. Dragging more volume into the right atrium with respiratory activity will not cause an inequality of ventricular filling (between the right and left ventricles) because the venous return will be “shared”.
Reversed splitting of S2
In this situation, P2 occurs before A2, and splitting widens during expiration (or inspiration in the mechanically ventilated patient). This only happens if the conduction to the left ventricle is delayed, or if the left ventricle is massively volume overload (and the right ventricle is not).
Left bundle branch block - the left ventricle depolarises after the right ventricle, and A2 is delayed
Aortic stenosis - the left ventricle empties slowly though a narrow valve
Large patent ductus arteriosus - the left ventricle receives a backflow of blood from the aorta, which causes it to become volume-overloaded
21.1 A patient with C6 tetraplegia is undergoing removal of bladder stones under general anaesthesia. The blood pressure rises to 166/88 mmHg. The appropriate response is to
a. Clonidine
b. Hydralazine
c. Decompress the bladder
d. Fentanyl
e. Deepen your anaesthetic
decompress the bladder
Autonomic Dysreflexia:
- medical emergency characterised by severe hypertension,
- brought on by stimulation below the level of the lesion
Factors affecting the development of ADR:
1. Level of spinal injury
2. Duration of injury
3. Whether injury is complete or incomplete
Pathology:
Stimuli arise from caudal roots below the level of the lesion leading to uncontrolled sympathetic activation below the level of the lesion
○ 80% being due to bladder distension
○ Other triggers include
§ bowel distension
§ acute abdo pathology
§ activation of pain fibres
§ sexual activity
§ uterine contractions
22.2 A 50-year-old man has the following pulmonary function test result: (provided). The most consistent diagnosis is
FEV1 68%, FVC 68%, DLCO 91%
a. Pulmonary hypertension
b. pulmonary fibrosis
c. myasthenia gravis
d. sarcoidosis
c. myasthenia gravis
21.2 A 25-year-old male has continued post operative bleeding after an extraction of an impacted third molar tooth under a general anaesthetic. The patient mentions that his father bruises quite easily. His coagulation screen reveals: (Coagulation tests provided). The most likely diagnosis is
His coagulation screen reveals: Prolonged APTT, Normal PT.
a) Factor V Leiden
b) Haemophilia A
c) Haemophilia B
d) Von willebrand disease
d) Von willebrand disease
- autosomal dominant inheritance
- may have normal or prolonged APTT, PT is normal
*Haem A: X-linked recessive disorder; would expect prolonged aPTT, and normal PT
*Haem B: X-linked recessive disorder; would expect normal aPTT and normal PT
Up to date:
Inheritance patterns — Most cases of VWD are transmitted as an autosomal dominant trait; this includes types 1 and 2B, and most types 2A and 2M.
Baseline hemostasis assessment —
Most patients will have a complete blood count (CBC) with platelet count and coagulation studies during the initial evaluation for excessive bleeding or bruising.
●Individuals with VWD generally have a normal CBC and a normal platelet count, with the exception of those with type 2B VWD, most of whom will have mild thrombocytopenia (eg, platelet count 100,000 to 140,000/microL).
●Individuals with VWD may have a normal or prolonged activated partial thromboplastin time (aPTT), depending on the degree of reduction of the factor VIII level. The prothrombin time (PT) is normal in VWD.
Up to date:
●Hemophilia A – Inherited deficiency of factor VIII (factor 8 [F8]); an X-linked recessive disorder.
●Hemophilia B – Inherited deficiency of factor IX (factor 9 [F9]); also called Christmas disease; an X-linked recessive disorder.
Laboratory findings —
Hemophilia is characterized by a prolonged activated partial thromboplastin time (aPTT).
However, the aPTT may be normal in individuals with milder factor deficiencies (eg, factor activity level >15 percent), especially in hemophilia B (factor IX deficiency), where even individuals with moderate disease may have a normal aPTT.
In some individuals with hemophilia A, factor VIII levels may increase with stress, leading to a normalization of the aPTT or mis-categorization of factor levels and disease severity.
In patients with hemophilia, the aPTT corrects in mixing studies, unless an inhibitor is present, which only applies to individuals who have received factor infusions or who have an autoantibody such as a lupus anticoagulant or an acquired factor inhibitor.
Mixing studies that do not show correction of a prolonged aPTT suggest an alternative diagnosis such as an acquired factor inhibitor.
The platelet count and prothrombin time (PT) are normal in hemophilia.
Thrombocytopenia and/or prolonged PT suggest another diagnosis instead of (or in addition to) hemophilia.
Measurement of the factor activity level (factor VIII in hemophilia A; factor IX in hemophilia B) shows a reduced level compared with controls (generally <40 percent).
One exception is an individual with mild hemophilia A who undergoes testing when stressed or pregnant and has a falsely elevated factor level. If this is suspected, factor activity testing should be repeated under conditions of low stress.
The plasma von Willebrand factor antigen (VWF:Ag) is normal in hemophilia.
If VWF:Ag is reduced, this suggests the possibility of von Willebrand disease (VWD) rather than (or in addition to) hemophilia.
Urinalysis is not done routinely, but if performed it may sometimes (but not always) show microscopic or macroscopic hematuria.
23.1 In a patient with glucose-6-phosphate dehydrogenase deficiency (G6PD), the
intravenous agent that should be avoided is
a. Methylene blue
b. Indocyanine green (ICG)
c. Iodine
d. Dextrose
a) methylene blue
Drugs to avoid:
Antibiotics
Sulphonamides (check with your doctor)
Co-trimoxazole (Bactrim, Septrin)
Dapsone
Chloramphenicol
Nitrofurantoin
Nalidixic acid
Antimalarials
Chloroquine
Hydroxychloroquine
Primaquine
Quinine
Mepacrine
Chemicals
Moth balls (naphthalene)
Methylene blue
Foods
Fava beans (also called broad beans)
Other drugs
Sulphasalazine
Methyldopa
Large doses of vitamin C
Hydralazine
Procainamide
Quinidine
Some anti-cancer drugs
20.1 The neurosurgical registrar has telephoned about a patient with a spinal cord tumour who is on the list for tomorrow. The registrar tells you the patient has Brown-Séquard syndrome (hemisection of the spinal cord). On clinical examination, below the level of the lesion, you would expect to find all EXCEPT ipsilateral
A. Hyperreflexia
B. Loss of tactile stimulation
C. Paralysis
D. Loss of pain/temperature
E. Loss of vibration/proprioception
D. Loss of pain/temperature
Brown-Sequard syndrome:
- Also known as Lateral hemi-section syndrome
- Causes
○ Common
§ Knife or bullet injuries
§ Demyelination
○ Rare
§ Spinal cord tumours
§ Disc herniation
§ Infarction
§ infection
Ipsilateral:
- Motor weakness
- Loss of vibration sensation
- Loss of proprioception sensation
Contralateral:
- Loss of pain sensation
- Loss of temperature
Segmental Syndrome:
- Pathologies that affect all functions of the spinal cord at one or more levels
- Total cord transection:
○ Cessation of function in all ascending and descending spinal cord pathways
○ Loss of all types of sensation below the level of the lesion
○ Loss of movement below the level of the lesion
- Acute transection:
○ Spinal shock
○ Flaccid paralysis
○ Urinary retention
○ Diminished tendon reflexes
○ This is usually temporary followed by:
§ Increased tone
§ Spasticity
§ Hyperrelfexia
§ supervene days or weeks after the event
- Transverse injuries above C3 involve sensation of respiration and are often fatal if acute
- Lesions above L2 will cause impotence and spastic paralysis of bladder
- Causes:
○ Myelopathies
§ Traumatic injury
§ Spinal cord haemorrhage
○ Epidural or intramedullary abscesses or tumours and transverse myelitis may have a more subacute presentation
Dorsal (posterior) cord syndrome:
- Bilateral involvement of:
○ Dorsal Columns
○ Corticospinal tracts
○ Descending central autonomic tracts to bladder control centres in the sacral cord
- Symptoms/signs:
○ Gait Ataxia (DC)
○ Paraesthesias (DC)
○ Weakness (CST)
§ Acute
□ Muscle flaccidity
□ Hyporeflexia
§ Chronic
□ Muscle hypertonia
□ Hyperreflexia
○ Extensor plantar response
○ Urinary incontinence (Auto)
- Causes:
○ MS
○ Tabes dorsalis
○ Friedrich ataxia
○ Sub-acute combined degeneration
○ Vascular malformations
○ Epidural and intradural extrameduallry tumours
○ Atlantoaxial subluxation
Ventral (anterior) cord syndrome
- Involves cords in the anterior 2/3rds of the spinal cord
○ Corticospinal tract
○ Spinothalamic tract
○ Descending autonomic tracts to the sacral centers for bladder control
- Signs/symptoms
○ Weakness (CST)
○ Reflex changes (CST)
○ B/L temp and pain sensation (Spino)
○ Tactile and vibratory sense are normal
○ Urinary incontinence (Auto)
- Causes:
○ Spinal cord infarction
○ Intervertebral disc herniation
○ Radiation myelopathy
23.1 A patient with long-term severe anorexia nervosa is commenced on a normal diet. Three days later she develops cardiac failure and exhibits a decreased level of consciousness. The most important parameter to assay and normalise is the plasma
a. Phosphate
b. Potassium
c. Magnesium
d. Sodium
e. Calcium
a) Phosphate
hypophosphate: Clinical symptoms range from muscle weakness and paraesthesia to severe cardiac failure, seizures and diaphragmatic paralysis
Refeeding malnourished patients with anorexia nervosa can be associated with hypophosphatemia, cardiac arrhythmia and delirium. Phosphorus repletion should be started early with and serum levels maintained above 3 mg/dL
weakness and fatigue, in the context of a recent history of starting a regular diet while in a state of chronic malnutrition, are concerning for refeeding syndrome, which typically occurs 2 to 5 days after beginning nutritional repletion. Depleted phosphate stores due to prolonged starvation, hypocalcemia, and hypokalemia can lead to impaired muscle contractility and subsequently weakness, myalgia, and tetany.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4168120/
22.1 A 26-year-old patient presents with exertional syncope. The most likely diagnosis is
a. HOCM
b. Long QT syndrome
c. CCF
d. IHD
HOCM: pathopneumonic
A person who has syncope during exertion is more likely to have an obstruction to blood flow (aortic stenosis or hypertrophic cardiomyopathy) or ventricular tachycardia as a cause. On the other hand, syncope after completion of exercise is more likely of reflex origin, such as the common faint.
https://www.uptodate.com/contents/syncope-fainting-beyond-the-basics#:~:text=A%20person%20who%20has%20syncope,such%20as%20the%20common%20faint
22.1 Created by the Global Initiative for Chronic Obstructive Lung Disease, the alphabetical GOLD groups A to D are tools for the assessment of chronic obstructive pulmonary disease. These classes are based on
a. Symptoms and exacerbations
b. FEV1
c. FEV1 and exacerbations
d. FEV1/FVC and exacerbations
e. FEV1 and symptoms
Sx and exacerbations
FEV1
GOLD ABE assessment tool
A 50-year-old man has the following pulmonary function test result. The most consistent diagnosis is
FEV1 98% predicted
FVC 98% predicted
DLCO 48% predicted
a) Asthma
b) Obesity
c) Sarcoidosis
d) Pulmonary hypertension
d) Pulmonary hypertension
Normal spirometry + low DLCO
Asthma: obstructive pattern and normal DLCO
Obesity: restrictive pattern and normal DLCO
Sarcoid: restrictive pattern and low DLCO
21.2 Cardiovascular effects of hyperthyroidism include
a) Increased DBP
b) Narrow pulse pressure
c) Reduced diastolic relaxation
d) Decreased CO
e) Decreased SVR
e) Decreased SVR
- increased CO, increased SBP and decreased DBP with widened PP
UP TO DATE: Cardiovascular effects of hyperthyroidism:
- Thyroid hormone has important effects on cardiac muscle, the peripheral circulation, and the sympathetic nervous system that alter cardiovascular hemodynamics in a predictable way in patients with hyperthyroidism.
- The main changes are :
●Increases in heart rate, cardiac contractility, systolic and mean pulmonary artery pressure, cardiac output, diastolic relaxation, and myocardial oxygen consumption
●Reductions in systemic vascular resistance and diastolic pressure
21.2 The risk of postoperative respiratory failure in myasthenia gravis is increased by the
administration of
a) Teicoplanin
b) Flucloxacillin
c) Cephazolin
d) Gentamicin
e) Vancomycin
d) Gentamicin
Drugs in the anaesthetic trolley that may unmask or worsen MG:
- NMBs
- gentamicin
- beta blockers (metoprolol)
- magnesium
Anaesthetic drugs to be cautious with:
- dexamethasone
- antipsychotics
- anticonvulsants
- antibiotics (vancomycin, metronidazole)