5Physical exam GA- A young female, looked pale, fatigue, cachexia. V/S- BP 214/150 mmHg, PR 124/min, RR 22 /minBP 4 extremities: / /143255/ /141HEENT- Marked pale, no jaundice, CLN-veNo engorged neck vein.Thyroid gland not enlarged.
6Heart- Active precordium. LV heaving- positive. PMI at 6th ICS, 2 cm Heart- Active precordium. LV heaving- positive. PMI at 6th ICS, 2 cm. lateral to MCL. Tachycardia, regular HR. No murmur.Lungs- Crepitation both basal lungs.Abdomen- Soft, liver and spleen not palpable. No renal bruit.Ext.- No edema. Equal pulses, no bounding pulse. No tremor, no moist skin.
7Neuro- E4M6V5. Pupils 3 mm RTL, BE. Eye ground- Blur disc with cotton wool spot with flame shape hemorrhage.Copper wire changes of vvs.CN intact all.Motor gr.V all. DTR 2+.BBK- plantar flexion both.Clonus- neg.
10CBC:Hb 11.3, Hct 33, WBC 11,800 ( N 68,L 19.1, Mo 10.1, Eo 1.4) Plt 136,000, MCV 82UA:Sp , pH 7.0, Alb 4+, Glu –ve, RBC 5-10, WBC 10-20, Hyaline cast 10-20,Granular cast 10-20, Epi 1-2BUN 14.8, Cr 1.8Elyte: Na 137, K 3.3, HCO3 25.6, Cl 106Ca 8.6, PO4 4.1, Mg 2.2LFT- Chol 201, Alb 3.7, Glob 3.6, TB 1.9, DB 0.2, ALT 16, AST 40, ALP 74
11Chest X-ray:LV hypertrophy, cephalization of pulmonary vein, Kerley’s B line.EKG-Sinus tachycardia, LVH by voltage, No LV strain patternFilm KUB- Not seen stoneUrine Elyte- Na 10, K 41.1, Cl 22Urine 24 hr- Cr 0.6, Prot 2,409 mg/vol,Vol= 760 ml. GFR= 23
12Serum osmole 287, Urine osm. 573TTKG = 6.2ANA – negativeAnti- HIV: Non reactiveTFT- FT ( pg/ml)FT ( ng/dL)TSH ( mIU/ml)
13Ultrasound KUBIncrease parenchymal echogenicity with loss of corticomedullary differentiation.Kidney size: Rt.9.15 cm., Lt cm.Cortical thickness: Rt cm., Lt cm.No hydronephrosis.
19Urine 24 hr. VMA27/04/ ug/mg Cr ( )28/04/ ug/mg Cr29/04/ ug/mg CrCT adrenal gland- Non enhancing posterior Lt. pararenal mass contains fat density.- Normal both adrenal glands.- Small liver nodule at segment 7 about 1 cm. in diameter.Imp: Lt. posterior pararenal mass contains fat density DDx retroperitoneal mass.
22Effects of HT (TOD) 3. Kidney - Atherosclerosis of afferent and efferent arteriole, glomerular capillary tufts- Decrease GFR, tubular dysfunction- Glomerular disease as a cause: proteinuria, microscopic hematuria
23Hypertensive emergency Diastolic BP > 120 mmHgSevere acute target organ damage- Hypertensive encephalopathy: severe headache, vomiting, visual disturbances, transient paralysis, convulsion, stupor, coma- Cardiac decompensation- Rapidly declining renal function
24Hypertensive emergency Vascular lesion- Fibrinoid necrosis of walls of small arteries arterioles- Cerebral arteries dilate excessive cerebral blood flowMicroangiopathic hemolytic anemia ( 2ry to deteriorate renal function)
25Hypertensive emergency: Management Rapid acting IV antihypertensive agent- Labetalol, Fenoldopam, Nitroprusside, Nimodipine- Decrease DBP 10-15% in < 1 hr.( not to level < 95 mmHg)IV nitrate + furosemide in acute pulmonary edemaCorrection underlying disease
26Hypertensive Retinopathy In 1939, Keith et. al. ----predictive of death in HT patientsClassification system: Keith-Wagener-Barker classification – categorized into 4 groups of increasing severitySigns of hypertensive retinopathy regress with control of BP
31Hypertensive nephrosclerosis Present with HT& its complications (eg, heart failure, stroke), and/or symptoms of uremia.Features suggesting HN :- Black race- Hypertensive retinal changes- Left ventricular hypertrophy- Long-standing (usually >10 y) or very severe hypertension- Proteinuria less than 0.5 g/d- Hypertension diagnosed prior to onset of proteinuria- Hypertension preceding renal dysfunction- No evidence of another renal disease- Biopsy findings compatible with the diagnosis
32Hypertensive nephrosclerosis - 30% present with declined GFR at presentation- Some patients with biopsy-proven HN have 24-hour urinary protein increase to the nephrotic range when secondary changes of FSGS present
33Glomeruli obsolescence, interstitial fibrosis, arterial intimal fibroplasia, arteriolar hyalinization in arteriolesGlomerular hyalinosis and the development of secondary tubular atrophy and interstitial fibrosisWrinkling of the glomerular tuft and thickening of the Bowman capsule
34Hypertensive nephrosclerosis Antihypertensive therapy and ACE inhibitor- Nephrosclerosis is part of generalized vascular disease- Patients with cardiovascular disease and impaired renal function benefit more than those with normal kidney function- BP control magnify long-term cardiovascular risk
362ry HT is suspicion 1. Age <35 or > 55 2. Therapeutic failure with initial drug program(3-drug rx.)3. BP >180/110 mmHg4. Sudden↑ BP in well-controlled HTN
372ry HT is suspicion 5. Signs & symptoms of specific disease - HA/palpitation/pallor/sweats- Renal bruits- SBP in legs < 20 mm SBP in arms- Cushing's physical stigmata6. Abnormal lab- K+ <3.5- Elevated creatinine- Elevated calcium- Abnormal UA
39Causes of 2ry HT Vascular cause - Coarctation of aorta Obstructive sleep apneaMedications: OCPs, Cocaine, EtOH
40Renal Parenchymal Disease Single largest cause of secondary hypertensionMost are irreversible.Acute renal failure- Acute glomerulonephritis (especially post-infectious, crescentic, or focal segmental changes)- Vasculitis (esp. SLE, scleroderma, or polyarteritis- Acute obstruction
42Chronic glomerulonephritis 1. Rapidly progressive glomerulonephritis (RPGN) or crescentic glomerulonephritis- 90% progress to ESRD within weeks or months.2. Focal segmental glomerulosclerosis (FSGS)- 80% progress to ESRD in 10 years- Collapsing variant: Malignant FSGS, have more rapid progression: Idiopathic or related to HIV infection.3. Membranous nephropathy% progress to chronic renal failure (CRF) and ESRD in 10 years.
43Chronic glomerulonephritis 4. Membranoproliferative glomerulonephritis (MPGN)- 40% progress to CRF and ESRD in 10 years.5. IgA nephropathy- 10% progress to CRF and ESRD in 10 years.6. Poststreptococcal glomerulonephritis- 1-2% progress to CRF and ESRD.- Older children or adults with crescentic glomerulonephritis are at greatest risk
44Chronic glomerulonephritis Hemodialysis + antihypertensive may increase survival in malignant hypertension associated with severely damaged renal functionDifficult to distinguish- HT is a consequence of nephritis or consequence of renal failure
45Renovascular HTFibromuscular dysplasia of renal arteries - About 25% of all renovascular HT- Young femalesAtherosclerotic disease- Nearly 70% of the total- Generally arise bilaterallyArteriography- gold standard: Critical stenoses of ≥80%
46Renovascular HTACE-inhibitor produces a fall GFR on the affected side.Positive scan correlates with successful angioplasty or surgical intervention in≥ 90% (less definitive in the presence of renal dysfunction)
47Hyperaldosteronism Primary hyperaldosteronism - Adenoma, carcinoma, or bilateral hyperplasia- Enzymatic deficiencies (11-OH-hydroxylase deficiency, 17-OH-hydroxylase deficiency, and 11-OH-dehydrogenase deficiency syndromes)- Chronic licorice ingestionNon-specific weakness, fatigue, polyuria, or cramps (reflecting hypokalemia)
48HyperaldosteronismBest screening test : 24-hour urinary collection for aldosteroneSimpler screening test : Plasma aldosterone to plasma renin activity (PRA) ratioPA/PRA ratio >30 and a PA >20 ng/ml(withdrawn from antihypertensive medications for ≥two weeks)
49Pheochromocytoma Nearly 80% of the tumors limited to adrenal glands - Usually unilaterally- Bilateral or multiple in neurofibromatosis, Von Hippel-Lindau disease, or MEN type 2a or 2b10-20% intra-abdominal sites, <5% from intrathoracic sites
50PheochromocytomaClassic triad : episodic headache, palpitations with or without tachycardia, and inappropriate perspirationDefinitive diagnosis and full localization requires both: Biochemical tests for catecholamines: Scanning potential sites by CT or MRI
51Medications- Vasoconstrictors : phenylephrine, pseudoephedrine, phenylpropanolamine, β-agonist bronchodilators, ephedrine, cocaine, stimulant abuse, anti-adrenergic agent withdrawal, and MAOI cotreatment with tyramine-containing foodsVolume expanders (glucocorticoids, estrogens at high doses, NSAIDSPoorly specified mechanisms such as cyclosporine, tacrolimus, or erythropoietinMiscellaneous other agents like psychotropic drugs that interfere with sympatholytic antihypertensive agents