TUT Flashcards
Splenomegaly
Has a notch
Non-ballotable
Can’t get above it
Moves inferior-medially
Enlarge towards umbilicus
Moves early on inspiration
Lower back pain (Red flags)
Neurological defect
Trauma
Previous surgery
Osteoporosis
Unexplained fever/weight-loss
Malignancy
Immunosuppression
Inflammatory nature of pain
Age (<20)
Prolonged use of corticosteroids
Acute onset or asthma
Cough
Wheeze
Increased Work of breathing
Restlessness
Anxiety
Hypoxia
Dyspnea
Tachycardia
Tachypnoea
Pulsus Paradoxs
Severe asthma
Exhaustion and fear
Inability to speak (Breathlessness)
Drowsiness (hypercapnia)
Cyanosis
Tachycardia (Hypoxemia)
Pulsus Paradoxs
‘Silent’ Chest
Left Ventricular Failure
Pulsus Alternans
Displaced, Dilated apex
S3
Bi-basal crackles
Pre-Renal failure (causes)
Dehydration
Shock
Sepsis
Drugs (NSAIDs, ACEi)
Pre-Renal failure (Dx/Signs)
Dehydration
History of [prev]
Mucosal membrane
Orthostatic HPT
Tachycardia
Urea: Creatinine ratio (7) (1:10)
Oliguria (improve with fluids)
Fraction excretion of Na (7)
Urine Na (<20 mm/mol)
TB on Abdo exam (Signs)
Weight-loss
Fever
Abdominal pain
Ascites
Hepatomegaly
Bowel obstruction
Diarrhea
Abdominal mass
‘Doughy’ abdomen
TB Abdo (Dx)
Ascites present = TB pleural effusion
SAAG <11
Lymphocytic with raised ADA
Ultrasound
Para-aortic lymph nodes
Micro-abscesses
Risk factors of Ischemic CVA
2nd(ary) = DM, HPT
Atherosclerosis (Angina, Claudification, Erectile dysfunction)
Previous Vascular event
Systemic (fever, arthritis, constitutional symptoms)
Lacunar stroke (Definition)
Lacunar infarcts are mostly caused by lipohyalinosis or microatheroma of a small penetrating endartery in basal ganglia or pons. Less than 25% of lacunar strokes are caused by large vessel artheroembolism.
Pericardial Effusion (Signs)
Absent apex beat
Muffled heart sound
Enlarged cardiac dullness
hypothyroidism
Face puffy
Skin (Cold, dry, rough) & Yellow discoloration
Hoarse voice
Bradycardia
Slow mentation
Slow reflexes
Concentration difficulties
S3
Rapid ventricular filling on opening of AV valves
Due to reduced ventricular compliance/diastolic overload
MI
TI
AI
VSD & PDA
Constrictive Pericarditis
S4
Due to high-pressure atrial wave reflected back from a poorly compliant ventricle
Atrial contraction with a “non-compliant” ventricle
Systolic overload/decreased compliance
AS
HPT & pulmonary HPT
HOCM (Hypertrophic Obstructive Cardiomyopathy)
Infarction/Ischemia
Acute AI/MI
3 Complications of TB on spine
Pott’s disease
Arachnoiditis
Transverse Myelitis
JVP vs Arterial
visible but not palpable
More prominent inward movement
Complex wave form
Moves on respiration (decreases on inspiration)
first obliterated than fills from above when light pressure is applied on the base of the neck
Bronchus carcinoma (Early disease detection)
Chronic cough
Blood stained sputum
LOW
Bronchus CA (direct invasion)
Chest pain
SOB
Hoarseness
SVC syndrome
Pathological fracture
Brain mets
Bronchus CA (paraneoplastic syndrome)
SIADH
HyperCa
Cushing’s
Hypoglycaemia
Acanthosis
Dermatomyositis
A good screening test
Cheap
Safe
Prevalence of the disease NB
Able to pick up pathology early (pre-symptomatic)
Treatable disease
Treatable with high mortality - sensitivity NB
Non-treatable - specificity NB
Paraneoplastic syndromes
not caused by direct infiltration of the malignancy. Effect is produced by hormones, cytokines or proteins secreted into circulation.
Weight loss, Fever (Unexpected)
First symptom of malignancy (when the primary is still to small to cause symptoms itself)
Signs of reccurrence
TMN Staging (Tumor)
T1 – <3cm
T2 – >3 cm
T3 – onto structures which can be surgically remove (ribbes)
T4 – less than 2cm from carina OR nodules in another lobe (same lung) OR onto structures that can not be surgically remove (aorta, pericardial, phrenicus)
TMN Staging (Nodes)
N1 – Hilar same side
N2 – hilar contralateral side / para-aortic
N3 - supraclavicular
TMN Staging (Metastasis)
M0 – none
M1a – malignant pleural effusion OR nodule in other lung
M1b – distal mets (Brain, Adrenals, Bone)
possible explanations for SOB
Pleural effusion
Pneumonia
COPD
5 signs of cirrhosis in chronic alcohol user.
Palmar erythema
Duputreyn’s
Spider Nevi
Gynecomastia
Testicular atrophy
Features other than seen on motor exam which will indicate spinal lesion.
Flaccid paralysis
sphincter impairment (bowel and bladder dysfunction)
Sensory level
Secondary causes of HPT and a clinical feature of each
Coarctation of aorta = HBP
Obstructive sleep apnea = Snoring
Cushing’s = central obesity
Pheochromocytoma = headaches
Renal parenchymal disease = familial hx of CKD
Primary Aldosteronism = hypokalemia
Pleural effusion (CXR)
Typical effusion with Meniscus sign (concave shape)
Pleural thickening (no typical meniscus sx, sharp angle), post TB
Signs of ILD
Cough (Dry)
Clubbing
Crackles (fine-insp. -> coarse)
Progressive dyspnoea
Decr. expansion
Underlying connective tissue dx (SLE, RA etc.)
Confirm ILD
Bronchoscope
Lung biopsy
CXR
PFT’s
Lacunar Presentations
Pure motor Hemiparesis
Pure sensory stroke
Ataxic-hemiparesis
Dysarthria-clumsy hand syndrome
Cinical significance of being
diagnosed with lacunar v MCA stroke
LCA (small disease atherosclerosis) you don’t have to look for an embolic event whereas in MCA it could be an embolic event/phenomenon.
3 ECG features of pulmonary HPT
P. Pulmonale
Dominant R-wave in V1
T-wave inversion V1-V3
Besides signs of bilateral UMN weakness, hyperreflexia, clonus and
hypertonia, what other 2 features indicate a spinal cord lesion
Incompetence (bladder) UMN bladder
Lhermitte’s sign
Spinal TB (Potts Dx)
Infect vertebrae
Collapse = pressure in spine + paraperisis
X-ray = Disc body, Endplate, Adjacent vertebrae
Malignancy: Vertebrae body (mostly)
Final Dx: MRI
UMN pattern
Arachnoiditis
TBM
Exudate around spinal cord at lumbar & sacral
Cause: dysfunction of nerve roots
LMN pattern
Transverse Myelitis
Not true infection of chord
Immunological reaction (Rheumatoid Fever)
Antibodies -> demyelination of cord with Multiple Sclerosis like lesion = paraparesis
Associated with inflammation of optic neuron & blindness ( Devic’s Disease)
Stable angina
Clinical dx
Typical hx
Patient with risk fx.
Plaque but no rupture
Unstable angina
Typical Hx
ECG change
No enzyme leak
Rupture of atheromatous plaque
What are the important aspects/features on History, Signs and Investigations
which could lead to a diagnosis of Diabetic Nephropathy?
Foamy urine
Chronic Hyperglycemia
Chronic kidney dx features (HPT)
Nephrotic syndrome
rapid progressive albuminuria
Urine studies (Urine: Albumin: Creatinine ratio = ≥ 30mg/g)
Kassmaul’s sign
Increase in JVP with inspiration
Constrictive pericarditis, Restrive cardiomyopathy, right HF, massive PE,
Pulmonary embolism (ECG)
Sinus tachycardia
Rt Axis
RV strain
Tall R wave in V1
Inverted T waves in V1-V3
Incomplete RBBB
S1Q3T3 pattern (15% cases)
Presenting features and clinical signs of Chronic Bilharzia Infection
Portal HPT, Intestinal polyposis, seizures, anemia, Cor pulmonale,
Liver disease
Bloody stool
Abdominal (RUQ) tenderness
Rash
Hepatosplenomegaly
Fever
Jaundice (prehepatic) signs
What are the differences in presentation and clinical signs between Chronic
Bilharzia and Liver Cirrhosis?
Bilharzia (PRE-HEPATIC)= Portal HPT (Varices, Ascites, Splenomegaly)
Liver Cirrhosis (HEPATIC) = Chronic liver disease (5)
Pericardial effusion (ecg) TB pericarditis
Small complexes
Pulsus alternans
Pericardial Tamponade
Distended neck veins
Tachycardia
Drop in BP
Pulsus Paradoxis
Irregularly irregular pulse
signs of an irregularly irregular pulse
A pulse with an irregular rhythm, completely irregular with no pattern.
Pulse deficit
Radial-femoral delay
Radius pulse + Femoral pulse = delay
Young pt (HPT)
Coarctattion of aorta
Corrigan’s sign
Radial pulse compressed until it disappears, lift 90° to body pulse returns but same pressure maintained in Radial artery.
Prominent carotid pulsations.
Aortic Incompetence/Regurge
mechanism or techniques to obtain an accurate history other than Socrates
Open questions
Eye contact
Allow patient to tell story in their own words
Empathy
No judgement
reasons HIV patients may default ARV treatment
Depression
Alcohol-substance abuse
Non-disclosure
Inadequate treatment literacy
Stockouts
Inaccessible clinics
High pill burden
Adverse effects
Frequent dosing
Charcot’s joint
Deformed, disorganized joints due to loss of proprioception or pain (or both) this leads to recurrent unnoticed injury to joint.
Diabetic AMYOTROPHY
DM pt = proximal neuropathy of lower limbs (weakness of hip flexors/adductors & knee extensors associated with inguinal and thigh pain.)
depressed deep tendon reflexes (quadriceps)
Uni/Bilateral
Onset abrupt/ more gradual (days to weeks)
Guillain barre syndrome (clinical features)
Progressive ascending weakness
Areflexia
Paresthesis
Autonomic features
Resp. failure
Prove that an effusion is due to TB
AFB’s on microscopy
Gene-Xpert
Culture positive
Predominantly lymphocytic effusion with raised ADA
Typical symptoms
Type 1 Respiratory failure
Resp system cannot adequately provide O2 to body leading to hypoxemia.
Type 2 Respiratory failure
Resp system cannot sufficiently remove CO2 from body leading to hypercapnia.
Murmur
Timing
Area of greatest intensity
Radiation
Loudness
Pitch
Transudates
Membrane intact
Incr. hydrostatic power
Decr. Oncotic
Decr. Concentration
HF, Renal Dx (nephro)
Decr. albumin
Prot: Serum prot <0.5
LDH:Serum LDH <0.6
Subarachnoid haemorrhage
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