1) Hypertension nephrosclerosis

2) Diabetes nephropathy

3) Polycystic kidney disease

4) Alport syndrome-an inherited disorder (usually X-linked) – destruction of glomeruli (chronic glomerulonephritis).

5) Gromeluronephritis

7) Family Hx of kidney disease

8) Smoking- causes artery calcification

9) Overuse of painkillers + allergic reactions to a/biotic

10) Obesity- ↑prevalence of DM and HTN

11) Premature birth- 1 in 5 premature infants (32 weeks) may have calcium deposits in nephrons- neprocalcinosis

12) Age- kidney function ↓ in older people

13) Trauma / accident

1. Aetiology + Epi of SLE- also explain other types --------Saree
2. DDx, Criteria for diagnosis of SLE
Clinical presentation of SLE ( in-text+otherwise)-----Chris
3. Investigations of SLE--------------------------------Yazid
4. Management of SLE------------------------------Maz
5. social effects of illness-------------------------- Alvin

Possible pathology in the heart shown in ECG?
P wave can only be normal, unusually tall or unusually broad
The QRS complex can only have 3 abnormalities- it can be too broad, too tall and may contain abnormal Q wave length
ST segment can only be normal, elevated or depressed
T wave can either be too tall or inverted.

In ACS
STEMIST elevation Deep Q waveT wave inversion
NSTEMIT wave inversion
Unstable anginaST depression

ECG CHANGES when MI strikes!!
0- 2 minà ECG can still be normal
2- 30 minà hyperacute T wave (beware)
Up to 2 hoursà ST elevation
6 hoursà elongation of Q wave
12 hoursà T wave inversion
48 hoursà ST returning to baseline
Days/ weeksà T wave back to normal. Q wave permanently elongated`


ECG changes STEMI (LOCATION)
Anterior -Anteroseptal à V1 – V3-Anterolateral à V4 – V6, AVL
Lateralà Lead I, AVL
Inferiorà Lead II, III and AVF
Posteriorà V1(Tall R wave), V2 (ST depression)

Definitionà-a syndrome characterized by rapid decline in glomerular filtration rate (hours to days), retention of nitrogenous waste products, and perturbation of extracellular fluid volume and electrolyte and acid-base homeostasis.-usually asymptomatic and diagnosed when biochemical monitoring of hospitalized patients reveals a recent increase in blood urea (BUN) and creatinine concentrations (Serum creatinine)- Classified into 3 catogoriesà Prerenalà Postrenalà Intrinsic
Pre-renal
àmost common form of ARF due to mild to moderate renal hypoperfusion.
àrapidly reversible upon restoration of renal blood flow and glomerular ultrafiltration pressure.
àAutoregulatory dilation of afferent arterioles is maximal at means systemic arterial blood pressures of 80mmHg and hypotension below this level is associated with precipitous decline in GFR.

Post-Renal
à Urinary tract obstruction, very infrequent, < 5% of all ARF
à Requires obstruction to urine flow between the external meatus and bladder neck, bilateral ureteric obstruction or unilateral ureteric obstruction in a patient with one functioning kidney.
àDuring the early stages of obstruction (hours to days), continued glomerular filtration leads to increased intraluminal pressure above the site of obstruction. As a result there is gradual distention of the proximal ureter, renal pelvis, calyces and a fall in GFR.

Intrinsic Renal ARF
à Can be further divided to 4 causesà Disease of larger renal vessels, diseases of the renal microcirculation and glomeruli, ischemic and nephrotoxic ARF, and tubulointerstitial inflammation.
à Difference from pre-renal ARFà hypoperfusion induces ischemic injury to renal parenchymal cells, particularly in tubular epithelium undergoing necrosis and apoptosis.
à With severe tubular injurym debris accumulates within tubules causing obstruction of fluid flow; tubules then dilate and compress nearby peritubular capillaries causing greater ischaemic damage.

Angiography (Radio contrast)
àIntrarenal vasoconstriction triggered by radiocontrast agents (contrast nephropathy). It induces ARF at prerenal stage, causing an acute fall in renal blood flow and GFR, (a relatively benign urine sediment, and a low fractional excretion of sodium). Severe cases may show clinical or pathologic evidence of ATN. Contrast nephropathy classically presents as an acute (onset within 24 to 48 h) but reversible (peak 3 to 5 days, resolution within 1 week) rise in blood urea nitrogen and creatinine and is most common in individuals with preexisting chronic renal insufficiency, diabetes mellitus, congestive heart failure, hypovolemia, or multiple myeloma. The syndrome appears to be dose-related, and its incidence is only slightly reduced in high-risk individuals by use of more expensive low osmolality, nonionic contrast agents

Patients with advanced atherosclerosis can develop ARF after manipulation of the aorta or renal arteries at surgery or angiography, following trauma, or, rarely, spontaneously due to embolization of cholesterol crystals to the renal vasculature (atheroembolic ARF). Cholesterol crystals lodge in small- and medium-sized arteries and incite a giant cell and fibrotic reaction in the vessel wall with narrowing or obstruction of the vessel lumen. Atheroembolic ARF is frequently irreversible. A myriad of structurally diverse pharmacologic agents induce ARF by triggering allergic interstitial nephritis, a disease characterized by infiltration of the tubulointerstitium by granulocytes (typically but not invariably eosinophils), macrophages, and/or lymphocytes and by interstitial edema. The most common offenders are antibiotics (e.g., penicillins, cephalosporins, trimethoprim, sulfonamides, rifampicin) and NSAIDs (Table 260-1).









Renal Vascular Hypertension
à In patient with atherosclerotic disease in aorta and peripheral arteries (15-25% with symptomatic lower limb atherosclerotic vascular disease has renal stenosis.
Renal stenosis reduces blood flow into kidneys thus activates RAAS. Causes Hypertension.
Hypertension causes RENAL Failure
àChronic hypertension leads to nephrosclerosis (arteriosclerosis of the kidney arteries). This reduces blood perfusion intrinsically in the kidneys and ischaemia.

Diabetes and Renal Failure
àHyperglycemia leads to glomerular hypertension and hyperfiltration, which in turn lead to deposition of protein in the mesangium. These protein deposits ultimately lead to sclerosis of the glomerulus and renal failure. Due to microalbuminurea.
à Diabetic vasculopathy, resulting in damaged arterioles in kidneys and hypoperfusion.

Effects of drug on Renal failure
-Direct toxicity to tubule epithelial cells and/or intratubular obstruction


NSAIDS, ACE- inhibitors and Angiotension 2 Receptor blockersà Inhibit renal prostaglandin biosynthesis and angiontensin 2 enzymeà inhibit vasodilation in arterioles to increase renal perfusion.

Causes of AF- pathophysiology and signs + symptoms

The principle of AFà any condition resulting in raised artrial pressure, increased atrial muscle mass, atrial fibrosis or inflammation and infiltration of the atrium may cause AF.
This includes systemic causes as well.

Cardiac and non-cardiac causes:-
Hypertension
Congestive heart failure
Coronary artery disease and myocardial infarction
Valvular heart disease
Cardiomyopathy: dilated, hypertrophic
Myocarditis and pericarditis
Wolff-Parkinson-White syndrome
Sick sinus syndrome
Cardiac tumours
Cardiac surgery
Familial tachyarrhythmia
(e.g. lone atrial fibrillation)
Thyrotoxicosis
Phaeochromocytoma
Acute and chronic pulmonary disease (pneumonia, chronic obstructive pulmonary disease)
Pulmonary vascular disease (pulmonary embolism)
Electrolyte disturbances (hypokalaemia)
Increased sympathetic tone (exercise, adrenergically mediated arrhythmia)
Increased parasympathetic tone (vagally induced and postprandial arrhythmia)
Alcohol abuse ('holiday heart' and long-term use)
Caffeine, smoking, recreational drug use

à Multiple re-entrant waveforms within the atria bombard the A V node, which becomes relatively refractive to conduction due to the frequency of upstream electrical activity. The AV node is continuously bombardedwith depolarization wavesof varying strength and depolarization spreads at irregular intervals down to the Bundle of His. (ALL OR NOTHING)How re-entrant waveforms occur? 3 mechanisms initiating and maintaining AF;àEnhanced automaticity in the left atrium extending to proximal portion of the pulmonary veins.à Electrical remodeling of the atria with resultant shortening of the atrial refractory period increases the duration and stability of AF. ‘AF begets AF’à In chronic AF, areas of functional conduction block further divide and maintain persistently chaotic electrical state.

AF occurs in 3 distinct clinical circumstances:àAs a primary arrhythmia in the absence of identifiable structural heart disease àAs a secondary arrhythmia in the absence of structural heart disease but in the presence of a systemic abnormality that predisposes the individual to the arrhythmia àAs a secondary arrhythmia associated with cardiac disease that affects the atria
3 Primary ways AF affects haemodynamic function include;- loss of atrial kick (synchronized atrial mechanical activity)- Irregularity of ventricular response- Inappropriate rapid heart rate.


Clinical Presentation
à Symptoms can be variable. About 30% patients are found to have AF incidentally with other findings.Usual complaintsà Palpitations, fatigue/ poor exercise tolerance, dyspnoea, chest pain, presyncope and generalized weakness.

àPhysical findingsà Pulse- Irregularly irregular rhythm.àHypotension and poor perfusionà caused by decrease in atrial filling pressures and decrease in stroke volumeà rate related or lack of normal atrial kick.à Congestive heart failure if presentà indicated by rales, jugular distension, peripheral oedema and a gallop due to rapid rate.à sign of embolization, including TIA, stroke and peripheral arterial embolization.

1. Diagnosis of HTN- target BP, dx, control------------------------Saree
2. Mx of HTN- drugs+non-pharm--------------------------------Yazid
3. Diagnosis of DM
- target blood sugar, post-prandial hyperglycaemia-------------Maz
4. Mx of DM- drugs+non-pharm----------------------------------Christine
5. Dx hyperlipidaemia + Mx
- target lipid profile
-pharm, non-pharm---------------------------------------------Alvin
6. Investigations- calculating cardiac risk factors-------------------Chris