Physical exam GA- A young female, looked pale, fatigue, cachexia. V/S- BP 214/150 mmHg, PR 124/min, RR 22 /min BP 4 extremities: 215/ / / /141 HEENT- Marked pale, no jaundice, CLN-ve No engorged neck vein. Thyroid gland not enlarged.
Heart- Active precordium. LV heaving- positive. PMI at 6 th 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.
Neuro- 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.
CBC: Hb 11.3, Hct 33, WBC 11,800 ( N 68,L 19.1, Mo 10.1, Eo 1.4) Plt 136,000, MCV 82 UA: Sp , pH 7.0, Alb 4+, Glu –ve, RBC 5-10, WBC 10-20, Hyaline cast 10-20, Granular cast 10-20, Epi 1-2 BUN 14.8, Cr 1.8 Elyte: Na 137, K 3.3, HCO3 25.6, Cl 106 Ca 8.6, PO4 4.1, Mg 2.2 LFT- Chol 201, Alb 3.7, Glob 3.6, TB 1.9, DB 0.2, ALT 16, AST 40, ALP 74
Chest X-ray: LV hypertrophy, cephalization of pulmonary vein, Kerley’s B line. EKG- Sinus tachycardia, LVH by voltage, No LV strain pattern Film KUB- Not seen stone Urine Elyte- Na 10, K 41.1, Cl 22 Urine 24 hr- Cr 0.6, Prot 2,409 mg/vol, Vol= 760 ml. GFR= 23
Serum osmole 287, Urine osm. 573 TTKG = 6.2 ANA – negative Anti- HIV: Non reactive TFT- FT ( pg/ml) FT ( ng/dL) TSH 5.21 ( mIU/ml)
Ultrasound KUB Increase parenchymal echogenicity with loss of corticomedullary differentiation. Kidney size: Rt.9.15 cm., Lt cm. Cortical thickness: Rt cm., Lt cm. No hydronephrosis.
Effects 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
Hypertensive emergency Diastolic BP > 120 mmHg Severe acute target organ damage - Hypertensive encephalopathy: severe headache, vomiting, visual disturbances, transient paralysis, convulsion, stupor, coma - Cardiac decompensation - Rapidly declining renal function
Hypertensive emergency Vascular lesion - Fibrinoid necrosis of walls of small arteries arterioles - Cerebral arteries dilate excessive cerebral blood flow Microangiopathic hemolytic anemia ( 2ry to deteriorate renal function)
Hypertensive 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 edema Correction underlying disease
Hypertensive Retinopathy In 1939, Keith et. al. ----predictive of death in HT patients Classification system: Keith-Wagener- Barker classification – categorized into 4 groups of increasing severity Signs of hypertensive retinopathy regress with control of BP
Hypertensive 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
Hypertensive 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
Glomeruli obsolescence, interstitial fibrosis, arterial intimal fibroplasia, arteriolar hyalinization in arterioles Wrinkling of the glomerular tuft and thickening of the Bowman capsule Glomerular hyalinosis and the development of secondary tubular atrophy and interstitial fibrosis
Hypertensive 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
Essential vs. Secondary HT
2ry HT is suspicion 1. Age Therapeutic failure with initial drug program(3-drug rx.) 3. BP >180/110 mmHg 4. Sudden ↑ BP in well-controlled HTN
2ry 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 stigmata 6. Abnormal lab - K+ <3.5 - Elevated creatinine - Elevated calcium - Abnormal UA
Causes of 2ry HT Vascular cause - Coarctation of aorta Obstructive sleep apnea Medications: OCPs, Cocaine, EtOH
Renal Parenchymal Disease Single largest cause of secondary hypertension Most are irreversible. Acute renal failure - Acute glomerulonephritis (especially post-infectious, crescentic, or focal segmental changes) - Vasculitis (esp. SLE, scleroderma, or polyarteritis - Acute obstruction
Chronic 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.
Chronic 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
Chronic glomerulonephritis Hemodialysis + antihypertensive may increase survival in malignant hypertension associated with severely damaged renal function Difficult to distinguish - HT is a consequence of nephritis or consequence of renal failure
Renovascular HT Fibromuscular dysplasia of renal arteries - About 25% of all renovascular HT - Young females Atherosclerotic disease - Nearly 70% of the total - Generally arise bilaterally Arteriography- gold standard : Critical stenoses of ≥80%
Renovascular HT ACE-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)
Hyperaldosteronism Best screening test : 24-hour urinary collection for aldosterone Simpler screening test : Plasma aldosterone to plasma renin activity (PRA) ratio PA/PRA ratio >30 and a PA >20 ng/ml (withdrawn from antihypertensive medications for ≥two weeks)
Pheochromocytoma 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 2b 10-20% intra-abdominal sites, <5% from intrathoracic sites
Pheochromocytoma Classic triad : episodic headache, palpitations with or without tachycardia, and inappropriate perspiration Definitive diagnosis and full localization requires both : Biochemical tests for catecholamines : Scanning potential sites by CT or MRI
Medications - Vasoconstrictors : phenylephrine, pseudoephedrine, phenylpropanolamine, β-agonist bronchodilators, ephedrine, cocaine, stimulant abuse, anti-adrenergic agent withdrawal, and MAOI cotreatment with tyramine-containing foods Volume expanders (glucocorticoids, estrogens at high doses, NSAIDS Poorly specified mechanisms such as cyclosporine, tacrolimus, or erythropoietin Miscellaneous other agents like psychotropic drugs that interfere with sympatholytic antihypertensive agents