CCE 2 Medicine revision Flashcards
DM
a) macrovascular complications
b) microvascular complications
a) CVA, IHD, PVD
b) Retinopathy, Neuropathy, Nephropathy
Genetic type associated with DMT1
HLA- DR3/4
3 things in DKA
- Ketoacidosis
- Osmotic diuresis
- Potassium imbalance
- Serum can be normal as balanced by kidneys
- Total- insufficient K+ in cells
Management of DKA
- Fluids
- Insulin (once K+ reached 3.3mmol)
- Glucose monitoring
- Potassium- correct & monitor
- Infection- treat
- Chart fluid balance
- Ketones
Atheroma pathophysiology
- Exposure of endothelium to LDLs, adhesion molecules etc…
- Adhesion molecules allow leukocytes to stick to arterial wall
- Blood monocytes oxidise LDL –> Foam cells
- Macrophage foam cells release cytokines –> smooth muscle cell migration (from media to intima) & smooth muscle proliferation
- FIbroblasts form protective CT capsule
ECG changes in NSTEMI
- ST depression
- T wave inversion
- Pathological Q wave
ECG leads, their territories and the artery
- Anterior/ Septal = LAD
- V1-V4,
- Lateral = Circumflex
- V5,V6, I, avL
- Inferior = RCA
- II, III, avF
Secondary prevention of ACS
Antiplatlet x2, Statin, ACEi, Betablocker
- Aspirin 75mg once daily
- Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
- Atorvastatin 80mg once daily
- ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
- Atenolol (or other beta blocker titrated as high as tolerated)
- Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Layers of the heart
Finding of pericarditis on ECG
Wide spread saddle shape ST elevation
NYHA grading
- Class 1: Ordinary physical activity doesn’t cause angina. Strenous activity does
- Class 2: SLight limitation of ordinary acitivity eg- climbing stairs
- Class 4: Marked limitiation of ordinary pysical activity eg: 100-200m on flat
- Class 4: Inability to carry any physical activit without discomfort
If someone presented with a ‘sore throat’ what differentials would you be thinking off and what organisms/ aetiology? Also consider symptoms
- Acute pharyngitis
- Group A strep- lack of cough
- Viral- cough
- Acute tonsilitis
- If bacterial- STREP A is common
- Quinsy
- Strep. pyrogens
- Common cold
- Rhinovirus common
- Rhino-sinitus
- Often viral, Strep. pneumoniae
- Acute bronchitis
- Viral (common)
- Infectious mono
- Splenomegaly, Spleen rupture (be aware!!)
- Maculopapular rash
What is Beck’s Triad
Sign of cardiac tamponade
- Hypotension
- Distended neck veins/ elevated JVP
- Muffled heart sounds
Management of acute HF
OMFG
- Oxygen
- Morphine
- Frusimide
- GTN- under cardio advice if BP stable
Classic triad of Aortic stenosis
- Dysponea
- Chest pain/ angina
- Syncope
Pathophysiolgy of asthma
- APC present to Th2 lymphocyte –> Activation of B cells to plasma cells producing IgE. Expression of IgE on mast cells
- Antigen cross links on IgE on mast cells –> degranulation
- Cytokines –> Inflammation
- Proteases –> Tissue damage
- Prostoglandins –> Vascular dilation
- Leukotrienes –> SMC
- Vasoactive amines –> SMC & vascular dilation
Eosinophils attracked to area
Treatment of asthma stepwise ladder
- Short acting beta agonist- Salbutamol
- Add low dose ICS
- Add LABA (salmeterol)
- Leukotriene receptor antagonist (motelukast) OR increase ICS to medium dose
- if no response to LABA consider stopping
- Specialist therapy
Treatment of acute asthma
- Oxygen
- Salbutamol nebs
- Hydrocortisone (IV) or PO Pred
- Ipatropium bromide (antimuscarinic) nebs
- Theophyline IV
Consider intubation and Abx if necessary
ABG in asthma
a) Initially
b) If person is tiring- THIS IS CONCERNING and suggests life threatening asthma
a) Respiratory alkalosis (as tachypnoea)
b) Normal pCO2 or hypoxia
Resp acidosis is a bad sign in asthma
Most common cause of pneumonia bacterial
Strep. pneumoniae
ARDS
a) What is it?
b) How does it initially present?
c) Berlin’s criteria for ARDS
d) What is often shown on the CXR?
Severe inflammatory reaction to lung damage with bilateral pulmonary infiltrates not accounted for by HF or fluid overload
Initially presents as RFT1 (can progress)
Berlin’s criteria: Acute onset, Resp failure <1 week after a known/suspected trigger, Decreased FiO2/PO2, Should exclude CHF, other causes
- Bilateral opacities (similar to pulmonary effusion)
Well’s score cut off
= 4
If low risk do D-dimer and if -ve –> go home
If D-dimer high then do CTPA
2 main divisions of lung cancer
- Non-small cell:
- SCC, Adenocarcinoma, Large cells
- Small cell:
- Contrains neurosecretory graunules –> neuroendocrine hormones
What type of inheritance is CF and where is the mutation?
What is the patho?
a) Autosomal recessive
b) CTFR gene deltaF508
c) ATP gated chloride channel absent/ defective on cell surface on epithelial cells –> thick & sticky secretions
Affects sweat glands- so excessive NaCl in sweat (here failure to reabsorb)
Exocrine glands- Hyperviscous mucus (reduced Cl- secretion –> increased Na reabsorption –> increased water absorption)