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JaundiceTranscribed from the lecture of Dr. NgoSection D 2011 - Mikey Silverman
Jaundice Yellow discoloration of the skin, sclera, and mucous membranes as a
result of an elevated serum bilirubin concentration. Learning Objectives
To review and understand bilirubin metabolism To learn the differential diagnosis of jaundice To learn the subjective and objective data to be gathered in a patient
with jaundice.
Differential Diagnosis (3 types) Isolated disorders of bilirubin metabolism
Unconjugated hyperbilirubinemia Increased bilirubin production
Hemolysis, ineffective erythropoiesis, blood transfusion, resorbption of hematomas
Decreased hepatocellular uptake Drugs (rifampicin), Glibert’s syndrome
Decreased conjugation Glibert’s syndrome, Crigler-Najjar syndrome
Conjugated or mixed hyperbilirubinemia Dubin-Johnson syndrome Rotor’s syndrome
Liver Disease Hepatocellular dysfunction
Acute or subacute hepatocellular disease Viral hepatitis, alcohol, drugs, hypotension, metabolic disorders
(Reye’s syndrome), pregnancy-related Chronic hepatocellular disease
Viral hepatitis, alcohol, autoimmune hepatitis, metabolic (hemochromatosis, Wilson disease, NAFLD)
Hepatic Disorders with prominent cholestasis Diffuse infiltrative disorders
Granulomatous diseases (TB, sarcoidosis, lymphoma), amyloidosis, malignancy
Inflammation of intrahepatic bile ducts Primary biliary cirrhosis, drugs (erythromycin, TMP-S)
Miscellaneous conditions Drugs (estrogens), TPN, bacterial infections
Obstruction of the Bile Ducts Choledocholithiasis – a stone found at the level of the common bile duct
Hindrance to bile flow Manifests with jaundice, fever, pain Cholesterol/pigment gallstones
Parasites Ascaris, chlonorchis
Diseases of the bile ducts Inflammation/infection (primary sclerosing cholangitis, AIDS
cholangiopathy, hepatic arterial chemotherapy, postsurgical stricture); neoplasms (cholangiocarcinoma)
Extrinsic compression of the biliary tree Neoplasms (pancreatic CA), pancreatitis, vascular enlargement
History Onset Progression Accompanying symptoms
Abdominal pain Fever Pruritis Stool/Urine color Weight loss Pallor GI bleeding
Alcohol consumption Blood transfusion Drug use/abuse Sexual partner/s Travel Family history
Physical Examination Jaundice
at least 51 mol for icteric sclera Vital signs Skin Lymphadenopathy Heart & lungs Abdomen – tenderness, mass, organomegaly, ascites Extremities Signs of Portal Hypertension
Splenomegaly – obliteration of Traub’s space Ascites – shifting dullness, puddle sign Leg edema Caput medusa
Stigmata of Liver Cirrhosis Spider angiomata Palmar erythema Gynecomastia Parotid gland enlargement Testicular atrophy Loss of body hair Dupuytren’s contracture
Liver Function Tests Hepatocellular necrosis
ALT, AST Synthetic Function
Albumin (hypoalbuminemia) Prothrombin time (prolonged)
Cholestasis Elevated:
Bilirubin Alkaline Phosphatase GGTP (together with elevated SGTP, can be sure it is a liver
dysfunction) 5’ Nucleotidase
Imaging studies Ultrasound / EUS MRI / MRCP CT scan PTC ERCP
Clinical Evaluation Jaundice with abdominal pain & fever
Hepatocelluar carcinoma Hepatobiliary TB Amoebic liver abscess Benign CBD obstruction with cholangitis (stone, stricture, ascaris) Malignant CBD obstruction with cholangitis (pancreatic CA) Acute pancreatitis
Jaundice with abdominal pain, no fever Benign CBD obstruction without cholangitis (stones, structures, ascaris) Malignant CBD obstruction without cholangitis (pancreatic CA) Hepatocellular CA Metastatic CA to the liver
Jaundice without abdominal pain, with fever Leptospirosis Typhoid fever Malaria Sepsis Collagen diseases
Jaundice without abdominal pain & fever Acute hepatitis (viral, drug, alcohol) Chronic hepatitis Cirrhosis Congenital hyperbilirubinemia Malignant Obstruction of CBD
Approach to Patients with Hematologic DiseaseSection D 2011 - Mikey Silverman
Findings Leading to hematological Consultation RBC – Anemia, Polycythemia, Nucleated RBC’s WBC – Leukopenia/Leukocytosis, Lymphocytosis, Immature
Granulocytes Platelets – Thrombocytosis/Thrombocytopenia Lymphadenopathy/Splenomegaly Others
Exaggerated bleeding: spontaneous/trauma related, abnormal PT/aPTT
Leg Pain/Deep Vein Thrombosis History
General symptoms Performance status Weight loss Fever Fatigue/malaise/lassitude Weakness
Specific Symptoms By system
Performance Status Determines the physiologic reserve of the patient
i.e. Karnofsky performance scaleRating Definition
100 Percent No evidence of disease
90 Percent Normal activity with minor signs of disease80 Percent Normal activity with effort; signs of disease70 Percent Cannot do normal activity but cares for self60 Percent Requires occasional assistance50 Percent Requires considerable assistance; frequent medical care40 Percent Disabled, requires special care30 Percent Severely disabled; hospitalization may be indicated20 Percent Very sick; hospitalization necessary for supportive treatment10 Percent Moribund0 Percent Death
General Symptoms Weight loss
Frequently seen in many serious diseases including primary hematologic entities
Significant unintentional weight loss (5% body weight over 6-12 months)
Fever Elevation of body
temperature that exceeds normal daily variation
Increase in the hypothalamic set point
Mean oral temp: 36.8 +/- 0.4oC
Occurs in: Early
manifestation of aggressive lymphoma/acute
leukemia Accompanying immunodeficiency Other malignancies
Fatigue/malaise/lassitude Difficult to assess Maybe explained by fever and muscle wasting in patients with severe
diseases Weakness
Accompany malignant processes Manifest as a general loss of strength/reduced capacity for exercise Hematologic disease
Myeloma/lymphoma: central/peripheral nervous system invasion/compression
Specific Symptoms Nervous system
Headache Paresthesias Confusion Impairment of consciousness
Eyes Conjunctival plethora Diplopia
Ears Vertigo Tinnitus
Neck Painless swelling Diffuse swelling of the face
Chest/Heart Dyspnea and palpitations Cough Chest pain
Nasopharynx, oropharynx, oral cavity Epistaxis Anosmia/olfactory hallucination Sore tongue Macroglossia Gingival hyperplasia Dryness of mouth Dysphagia
Gastrointestinal system Abdominal fullness/discomfort Malabsorption Diarrhea Constipation
GU/Reproductive system Impotence/bladder dysfunction Hematuria Priapism Menorrhagia
Back/Extremeties Arthritis Hemarthroses Bone pain
Skin Pallor Bronze/grayish pigmentation
Cyanosis Jaundice Erythromelalgia Pruritus Petechia/ecchymoses
Personal and Environmental History Drug History Sexual History Occupational Exposure
Benzenes Organophosphates Herbicides
Nutrition Dietary deficiencies
Family History Hematologic disorders
Jaundice History of gallstones History of venous thromboembolism History of hemophilia
Ethnic background Past Medical History
Operations Previous transfusions
Physical Examination Pertinent body systems
Skin Pallor/flushing
Skin color is caused by the pigment contained therein and by the blood flowing through the capillaries
Mucous membranes, conjunctivae, palmar creases Cyanosis
Function of total amount of reduced hemoglobin May be influenced by skin pigmentation
Jaundice Observed in the skin of individuals who are not otherwise deeply
pigmented Caused by ble pigment (direct/conjugated bile)
Petechiae Small (1-2mm) round lesions from hemorrhages into the skin Present in areas of high venous pressures No blanching on pressure
Ecchymoses Various shapes and sizes Blanches with pressure
Excoriations Nails
Koilonchia Eyes
Jaundice Pallor Retinal hemorrhages/exudates Dilation of veins
Mouth Pallor Ulceration of oral mucosa Bleeding Tongue: macroglossia
Lymph nodes Cervical,
supraclavicular, axillary, epitrochlear, inguinal, femoral
EXTENT (localized/generalized)
SIZE TEXTURE TENDERNESS
Skeleton Spleen
Usually non palpable Other methods:
Traube’s Nixon’s Castelo
Liver Nervous system
Cerebral impairment, visual impairment, cranial nerve dysfunciton
POEMS (polyneuropathy, organomegaly, endocrinopathy, multiple myeloma, skin changes)
Joints Deformities: repeated hemorrhages
Edema/Urinary Complaints/Female GenitaliaSection D 2011 - Mikey Silverman
I. Approach to patient with kidney and urinary tract diseaseII. Edema
III. Discolored Urine – hematuriaIV. Abnormalities of Urine VolumeV. Renal and Ureteric Colic
VI. Symptoms related to the act of urinationVII. Symptoms of bladder outlet obstruction/prostatism
VIII. Urinary incontinenceIX. Female genital examination
I. Approach to Patient With Kidney and Urinary Tract disease Primary renal disease Secondary renal disease Disease of the urinary tract
Anatomic localization of the Lesion Kidneys
Glomerulus Tubules Interstitium Vascular System
Lower urinary tract Ureter Bladder Urethra
Cross-section of the kidney
Means of Discovery1. Symptomatology2. PE3. Laboratory abnormalities
II. Edema Palpable swelling produced by expansion of the interstitial fluid volume Localized or generalized ANASARCA – gross, generalized edema Recognized in its generalized form by puffiness of the face and
indentation of the skin following pressure (pitting edema)
2 basic steps for edema formation:1. Alteration in capillary hemodynamics2. Dietary Na and water retention by the kidneys
Major causes of edema according to primary mechanism 1. Increased capillary hydraulic pressure
Increased plasma volume due to renal Na+ retention Heart failure, including cor pulmonale
Primary renal sodium retention Renal disease, including the nephrotic syndrome Drugs: minoxidil, diazoixide, thiazoilidinediones, calcium channel
blockers, NSAIDs, fludrocortisone, estrogens Early hepatic cirrhosis
Pregnancy and premenstrual edema Idiopathic edema
Venous obstruction Cirrhosis or hepatic venous obstruction Acute pulmonary edema Local venous obstruction
2. Hypoalbuminemia Protein loss
Nephrotic syndrome Protein-losing enteropathy
Reduced albumin synthesis Liver disease Malnutrition
3. Increased capillary permeability Idiopathic edema Burns Trauma Inflammation or sepsis Allergic reaction, including certain forms of angioedema Adult respiratory distress syndrome Diabetes mellitus Interleukin-2 therapy Malignant ascites
4. Lymphatic obstruction or increased interstitial oncotic pressure Postmastectomy Nodal enlargement due to malignancy Hypothyroidism Malignant ascites
5. Uncertain mechanism Docetaxel Pramipexole
History Where is the edema located? Is the edema persistent or intermittent? Is the edema unilateral or bilateral? Is the edema pitting or non-pitting? Is there a history of any disorder or drug intake that can cause cardiac,
hepatic, renal disease? Pitting edema
Depression that does not rapidly refill and resume its original contour Reflects movement of excess water in response to pressure
Non-pitting edema Lymphedema Pre-tibial myxedema
Principal causes of Generalized Edema
Cardiac
Dyspnea on exertion, orthopnea, PND; edema extensive in the legs and accentuated in the evening
Elevated JVP, S3 gallop, occasionally with displaced or dyskinetic apical pulse, peripheral cyanosis, cool extremities, small pulse pressure when severe
Hepatic
Dyspnea infrequent, except if associated with significant degree of ascites, ethanol abuse
Ascites, JVP normal or low, BP lower than in renal or cardiac disease, signs of chronic liver disease – stigmata of cirrhosis
Renal
Usually chronic, may be associated with uremia – decreased appetite, metallic or fishy taste, altered sleep pattern, difficulty concentrating, restless legs, dyspnea may be present, but less severe than heart failure, bubbly urine
BP may be high, hypertensive or diabetic nephropathy, periorbital edema, pericardial friction rub, nitrogenous fetor, asterexis in uremia
Nephrotic syndrome Periorbital/peripheral edema Ascites Bubbly urine BP normal or elevated CVP normal to high normal Heavy proteinuria (>3.5 g/day) Hypoalbuminemia Lipiduria Hyperlipidemia
III. Discolored Urine – Hematuria Color Pathologic Non-pathologic
White ChylePus
Phosphates
Yellow to orange Bilirubin Concentrated urine
Urobilin RifampicinFood colorCarrotsNitrofurantoin
Read to brown to purple
PorphobilinPorphobilinogenUroporphyrinGlomerular DiseasesExtraglomerular diseases Hemoglobinuria Myoglobinuria
Natural food pigments (beets)Artificial food coloringPhenothiazinesPhenazopyridinesLaxatives(phenolpthalein, senna)
Blue to green
BiliverdinPseudomonas infection
Vitamin B complexPhenyl salicylatesThymolTriamtereneAmvtriptyline
Hematuria Macroscopic (grossly visible) – red or brown urine Microscopic (urinalysis) - >/- 2 RBCs/hpf Origin
Kidney – glomerulus – dysmorphic RBC Ureter Bladder Prostate Urethra Clotting mechanism defect
Etiology
History Color Transient or persistent Partial or total
Partial Initial – anterior urethral lesion (urethritis, stricture, meatal
stenosis) Terminal – posterior urethra, bladder neck, prostate
Total (throughout urination) Above the level of the bladder (stones, tumor, TB, nephritis)
Associated symptoms Frequency, dysuria, urgency, suprapubic pain Flank or CVA pain Passage of wormlike clots
Painful or painless Painless hematuria
Bladder or kidney tumor Polycystic kidneys Acute GN Sickle cell disease Tuberculosis Post-traumatic Post-exercise
Painful hematuria Stones Urinary tract infection Renal infarction
Ingestion of foods containing red vegetable dyes (beets) Medications: aspirin, anticoagulants, laxatives History of recent upper respiratory tract infection Positive family history of renal disease – polycystic kidney disease,
sickle cell, blood dyscrasia Recent vigorous exercise or trauma Travel or residence in areas endemic for Schistosoma haematobium,
or tuberculosis Cyclic hematuria – passage of hematuria during or after menstruation
PE Pallor Petechiae, echymoses, lymphadenopathy, splenomegaly – blood
dyscrasia CVA tenderness and fever – renal infarction Suprapubic tenderness – bladder
Bilaterally enlarged kidneys – PKD AF/valvular heart disease – renal embolism/infarction
IV. Abnormalities of Urine Volume Oliguria/Anuria
Normal load of metabolic waste product cannot be excreted Oliguria – 24-h urine output of < 400-500 mL/day Anuria – complete absence of urine < 50 mL/day Azotemia – retention of nitrogenous waste products (asymptomatic) Uremia – signs and symptoms brought about by azotemia (elevated BUN
and creatinine) dialysis Etiology
Acute renal failure Pre-renal Renal Post-renal
Chronic renal failure (> 3 months; irreversible) Note: non-oliguric renal failure – urine output of >500 mL/day with
acute or chronic azotemia Location of the Cause?
Clinical assessment of ARF Search for reversible factors that may be exacerbating ARF, e.g.,
hypervolemia, ongoing administration of nephrotoxic medications Examine for clinical evidence of uremia (e.g., asterixis, confusion, hiccups,
nausea, vomiting, pericarditis) Clinical assessment of intravascular volume Review most recent laboratory results for metabolic complications:
hyperkalemia, acidosis, hyperphosphatemia Review drug prescription: discontinue all non-essential drugs and adjust
dose or dose interval of drugs eliminated by kidney Review nutritional status: consider protein, salt, potassium and phosphate
restriction: consider need for enteral nutrition or hyperalimentation
Polyuria More than 3L urine/day Etiology
Excretion of non-absorbable solutes (osmolar loads) – glucose, mannitol
Excretion of water – defect in ADH production or renal responsiveness (diabetes insipidus)
History Symptoms of uncontrolled DM Intake of medications
PE – state of hydration
V. Renal and Ureteric Colic Renal Colic
Dull, aching, steady pain in the CVA just lateral to the sacrospinalis muscle and just below the 12th rib
Often unilateral Severe crescendo/decrescendo type of pain Radiates from CVA to hypochondrium (umbilicus) Due to sudden distention of the renal capsule Acute pyelonephritis Acute ureteral obstruction
Ureteral colic Similar characteristic as renal colic Severe colicky back pain that radiates from CVA towards inguinal
ligament into the scrotum or labia majora Acute obstruction – passage of a stone or blood clots
Ureteral stone Proximal ureteral stone – lateral flank to abdominal region; pain
radiates to the testicle (T11-12) Mid portion of the ureter, R side – pain radiates to the McBurney’s
point Midportion of the ureter, L – LLQ Distal ureteral stone – pelvis to inguinal canal/inner
thigh/groin/genitalia Ureterovesical junction – bladder irritability (frequency, urgency)
Caliceal stone Asymptomatic Small, non-obstructing Gross hematuria
Renal pelvis stone Asymptomatic Flank/CVA pain (ureteropelvic junction)
Stones – history Age of onset Family history of stone Fractures/immobilization – hypercalcemia Previous UTI or manipulation Renal or ureteric colic Associated symptoms – nausea, vomiting
Fever and chills (UTI) Gross hematuria – stone passage
Dietary habits/fluid intake Stones – PE
Flank tenderness Tophi
VI. Symptoms related to the act of urination Dysuria
Painful urination Tingling or burning sensation in the perineum during or just after voiding Caused by one of the 2 conditions
Inflammation involving the urethra and bladder trigone Inflammation involving the vaginal labia
Etiology Etiology Location Lower UTI (bacterial) bladder and urethra Acute pyelonephritis upper urinary tract Chlamydial urethritis urethra Gonococcal urethritis urethra Other urethritis urethra No recognized pathogen urethra Vaginitis vagina
History Onset of symptoms Nature of symptoms
Pain intensity Timing
Initial/during urinationUrethritisUrethral obstructionMeatal ulcer
TerminalCystitis (with dull and steady suprapubic pain)Bladder calculiProstatitis/seminal vasculitis
Localization Associated Symptoms
Frequency Nocturia Incontinence Hematuria Pelvic/back pain Fever/chills Vaginal discharge
Last menstrual period Sexual activity, type of contraception, symptoms in partner History of prior urinary or gynecologic symptoms and infections Conditions which might predispose to treatment failure (diabetes,
pregnancy, recent antibiotic treatment, hospitalization, urological instrumentation, urological anatomic anomaly)
Allergy to medications PE
Abdominal examination CVA tenderness – acute pyelonephritis Suprapubic tenderness – cystitis
Genital exam Prostate exam
Frequency Frequent voiding without increased urine flow Decreased voiding interval (<2 hours) Pollakuria – abnormal increased frequency of urination The normal capacity of the bladder is 400 mL Etiology
Residual urine – reduces the functional capacity of the organ Bladder inflammation – infection, stones, tumor Bladder fibrosis – TB, radiation cystitis, interstitial cystitis,
schistosomiasis Urgency
Sudden and compelling desire to pass urine that is difficult to defer Nocturia
Waking at night from sleep to void (>/= 2x) May be a symptom of renal disease due to a decrease in the function of
renal parenchyma with loss of concentrating power Can occur in the absence of disease History
On average, how many times do you wake up at night to void? Fluid intake (24 hour, bedtime, diuretic fluids) Medications (diuretics, xanthines, beta-blockers, cholinesterase
inhibitors) Co-morbid conditions Associated symptoms
Obstructive –hesitancy, weak urinary stream, incomplete emptying, intermittency)
Irritative – frequency, urgency, urinary incontinence PE
Comprehensive PE Enuresis
Nocturnal urinary incontinence Nighttime bed wetting Physiologic during the first 2-3 years of life May be functional or due to delayed neuromuscular maturation of the
urethrovesical component May also be a symptom of organic disease (UTI, distal urethral stenosis
in girls, posterior urethral valves in boys, neurogenic bladder)
VII. Symptoms of Bladder Outlet Obstruction/Prostatism Obstructive symptoms
Hesitancy Loss of force and decrease caliber of urinary stream (weak stream) Dribbling Abdominal straining Intermittency Acute urinary retention Chronic urinary retention Sense of residual urine Cystitis
Prostatism Syndrome which occurs with progressive vesicle obstruction Stages:
1. Early stage (irritability) Bladder musculature begins to hypertrophy Contraction of hypertrophied detrusor muscle is so strong, causing
spasm Urgency and frequency
2. Stage of compensation Obstruction increases, further hypertrophy of bladder musculature Bladder develops contractions strong enough to overcome
resistance at the bladder neck Exhaustion of the detrusor muscle as it nears end of the contraction
phase Urgency and frequency plus hesitancy, loss in force and size of
urinary3. Stage of decompensation
Bladder tone becomes impaired Urethral resistance exceeds detrusor power Inability of the bladder to contract and expel the contents of the
bladder Marked hesitancy, need for straining to initiate urination, very weak
and small stream, acute urinary retention, residual urine, overflow incontinence
Differential diagnosis Obstructive
BPH/prostate CA Vesical neck obstruction Urethral stricture
Functional Detrusor neuromuscular dysfunction Detrusor instability Psychogenic voiding dysfunction
Infectious and Neoplastic Cystitis Bladder CA Prostatitis Prostatic abscess
PE Enlarged kidneys – CVA mass CVA tenderness – infection Palpable bladder – distended bladder Palpation of the urethra – induration (stricture) DRE (Digital rectal examination)
Atony of anal sphincter Enlarged prostate Tender prostate (prostatitis)
Palpation of the posterior surface of the prostate gland. Feel for the lateral lobes and median sulcus
Enlarged Prostate
VIII. Urinary Incontinence Involuntary leakage of urine Urgency – sudden and compelling desire to pass urine that is difficult to
defer Urge Incontinence
Inability to hold urine once the urge to void occurs Secondary to involuntary bladder contractions Causes: cystitis
CNS disorder – upper motor neuron lesion Can be seen in tense, anxious women in the absence of infection
Stress Incontinence Leakage of urine due to increased intraabdominal pressure Involuntary leakage with coughing, sneezing, laughing, running Causes: weakness of bladder neck supports (pelvic floor relaxation);
urethral sphincter damage Unusual in nulliparous women
Overflow incontinence Paradoxical incontinence Loss of urine due to chronic urinary retention or secondary to a flaccid
bladder Mechanical dysfunction resulting from an overdistended bladder Causes
Anatomic obstruction by prostatic hypertrophy and strictures Neurologic abnormalities that impair detrusor contractility (multiple
sclerosis); spinal lesions Symptoms
Weak urinary stream Dribbling Hesitancy Frequency Nocturia
Functional Incontinence Intact urinary tract but factors like cognitive abilities, immobility, or
musculoskeletal impairments lead to incontinence Organic dementia, psychiatric patients
Patients may have more than one type of incontinence at any given time History
Onset and course of incontinence Associated lower urinary tract symptoms Leakage frequency, timing, volume Precipitants (medications, caffeinated beverages, coughing, laughing,
physical activity) Bowel and sexual function Status of other medical conditions and symptoms, along with their
temporal relationship to urinary incontinence onset or worsening Any prior incontinence treatment – surgery Have you leaked urine in the past 3 months? Which precipitants led to leakage? Which precipitant caused leakage most often?
PE Comprehensive PE Abdominal examination – to look for masses and tenderness, distended
bladder Rectal examination – to check for masses and impaction, prostate
consistency and symmetry Genital examination in women – to assess adequacy of pelvic support; to
assess presence of rectocoele, cystocoele
IX. Female Genital Examination External Examination
Inspection and Palpation
Labia Majora Labia Minora Clitoris Urethral orifice Vaginal introitus Skene and bartholin glands Muscle Tone
Draped patient in dorsal lithotomy position
Separation of the Labia
Palpation of Skene Glands Palpation of Bartholin Glands
Palpating the Perineum
Cystocele Rectocele
Internal Examination Use a speculum – cervix
Bimanual Examination Cervix Uterus Adnexa and ovaries
Rectovaginal examination Anal sphincter Rectal walls and rectovaginal septum
Examination of internal genitalia with speculum
Bimanual palpation of the uterus
Bimanual palpation of adnexa, sweep abdominal fingers downward to capture ovary
Rectovaginal Examination Anal sphincter Rectal walls and rectovaginal septum Uterus Adnexa Stool
Rectovaginal examination