Urine and stool examination
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Do you want urine and stool examination as:
- Routine laboratory tests
- Specimen collection and procedure
- Interpretation of normal and abnormal findings
- Exam notes with tables and key points
Create a table of normal and abnormal findings
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urinalysis AND fecal examination
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urinalysis normal values stool examination normal findings laboratory manual
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Urine examination
| Parameter | Normal finding | Abnormal finding | Possible significance |
|---|---|---|---|
| Colour | Pale yellow to amber | Dark yellow, red/pink, brown, orange, milky | Dehydration; blood/hemoglobin; bilirubin; drugs/foods; pus or crystals |
| Appearance | Clear | Cloudy/turbid | Cells, bacteria, crystals, mucus, or contamination |
| Odour | Slightly aromatic | Foul, fruity, ammoniacal | UTI; ketones in diabetes/starvation; old specimen |
| Specific gravity | About 1.005-1.030 | Low or high | Low: dilute urine or impaired concentrating ability. High: dehydration, glucose, protein, contrast media |
| pH | About 4.5-8.0, usually acidic | Persistently alkaline or markedly acidic | Alkaline: old specimen, urease-producing UTI, vegetarian diet. Acidic: ketoacidosis, diarrhea, high-protein diet |
| Protein/albumin | Negative or trace | Proteinuria | Renal disease, fever, strenuous exercise, pre-eclampsia |
| Glucose | Negative | Glycosuria | Diabetes mellitus; rarely renal tubular disorders |
| Ketones | Negative | Ketonuria | Diabetic ketoacidosis, prolonged fasting, vomiting, starvation |
| Bilirubin | Negative | Bilirubinuria | Conjugated hyperbilirubinemia, hepatobiliary obstruction or liver disease |
| Urobilinogen | Small amount may be present | Increased or absent | Increased: hemolysis or liver disease. Absent/low: complete biliary obstruction |
| Blood/hemoglobin | Negative | Hematuria or hemoglobinuria | Stones, UTI, trauma, glomerular disease, tumor; hemolysis if hemoglobinuria |
| Nitrite | Negative | Positive | Suggests nitrate-reducing bacterial UTI |
| Leukocyte esterase | Negative | Positive | Pyuria, usually UTI or urinary inflammation |
| RBCs, microscopy | None to few, commonly 0-2/HPF | Increased RBCs | Hematuria from infection, stone, glomerular disease, malignancy, menstruation contamination |
| WBCs/pus cells | Usually 0-5/HPF | Increased WBCs | UTI, interstitial nephritis, urinary inflammation |
| Epithelial cells | Few squamous cells | Numerous squamous or renal tubular cells | Squamous: contamination. Renal tubular cells: tubular injury |
| Casts | None, or occasional hyaline casts | RBC, WBC, granular, waxy, epithelial casts | RBC: glomerulonephritis. WBC: pyelonephritis/interstitial nephritis. Granular/epithelial: tubular injury. Waxy: chronic renal disease |
| Crystals | May be absent or occasional | Numerous or characteristic crystals | May suggest stone risk or metabolic disorder, depending on type |
| Bacteria/yeast/parasites | Absent | Present | UTI, candiduria, or contamination. Confirm suspected UTI with culture |
Typical dipstick findings include clear urine with negative protein, glucose, ketones, blood, leukocyte esterase, nitrite, and bilirubin, but the laboratory reference range on the individual report should be used. Urinalysis reference
Stool examination
| Parameter | Normal finding | Abnormal finding | Possible significance |
|---|---|---|---|
| Colour | Brown | Black/tarry, red, pale/clay, green, yellow/greasy | Black tarry: upper GI bleeding or iron/bismuth. Red: lower GI bleeding. Pale: reduced bile flow. Yellow/greasy: fat malabsorption |
| Consistency | Soft, formed | Watery, loose, hard, greasy/bulky | Watery: diarrhea/infection. Hard: constipation. Greasy/bulky: steatorrhea, pancreatic insufficiency, malabsorption |
| Frequency | Variable, often 1-3 times/day to 3/week | Persistent diarrhea or constipation | Infection, dietary/drug causes, functional or organic bowel disease |
| Mucus | Absent or minimal | Visible mucus | Colitis, inflammatory bowel disease, dysentery, infection |
| Visible blood | Absent | Fresh red blood or altered dark blood | Hemorrhoids, fissure, colitis, diverticular disease, colorectal lesion, GI bleeding |
| Occult blood test | Negative | Positive | Gastrointestinal bleeding, including colorectal neoplasia, ulcers, or inflammation. Requires clinical follow-up |
| Pus cells/WBCs | Absent | Present | Invasive bacterial diarrhea or inflammatory colitis |
| RBCs, microscopy | Absent | Present | Dysentery, invasive infection, inflammatory bowel disease, ischemic colitis |
| Ova, cysts, trophozoites | Absent | Parasite forms present | Intestinal parasitic infection, such as amoebiasis or helminthiasis |
| Bacterial culture | No enteric pathogen isolated | Pathogen isolated | Bacterial gastroenteritis, depending on organism and symptoms |
| Fat globules | Absent or scant | Increased fecal fat | Malabsorption, pancreatic exocrine insufficiency, celiac disease |
| Undigested muscle fibers | Absent or scant | Increased fibers (creatorrhea) | Pancreatic insufficiency or rapid intestinal transit |
| Reducing substances | Negative, especially after infancy | Positive | Carbohydrate malabsorption, most useful in pediatric assessment |
| Stool pH | Usually neutral to mildly acidic | Low pH, often <5.5 | Carbohydrate malabsorption with acidic diarrhea |
| Yeast | Usually absent/scant | Numerous yeast cells | May occur after antibiotics or with altered gut flora; interpretation needs symptoms and context |
Important: A single abnormal finding does not establish a diagnosis. Sample collection, diet, medications, menstruation, hydration, and delay in processing can alter both urine and stool results. Black, tarry stool, visible blood in stool or urine, or urine with fever/flank pain should be assessed promptly.
If the stool has foul smell
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A foul-smelling stool can occur with a dietary change, but if it is persistently very offensive it may suggest:
| Associated finding | Possible cause |
|---|---|
| Bulky, pale, greasy, floating stool that is hard to flush | Fat malabsorption (steatorrhea), such as pancreatic insufficiency, celiac disease, or impaired bile flow |
| Watery diarrhea, bloating, cramps, and excess gas, especially after unsafe water exposure | Giardiasis or another intestinal infection |
| Chronic diarrhea and weight loss | Malabsorption or chronic intestinal disease |
| Blood, mucus, fever, or severe abdominal pain | Invasive intestinal infection or inflammatory bowel disease |
| Black tarry stool | Possible gastrointestinal bleeding, needing urgent assessment |
Stools with steatorrhea are classically bulky, greasy, floating, and foul-smelling. Henry's Clinical Diagnosis and Management by Laboratory Methods notes that this pattern is characteristic of excess fat in stool. Foul-smelling diarrhea with flatulence lasting more than 2 weeks merits testing for Giardia.
See a clinician if the smell persists for more than a few days or occurs with weight loss, fever, dehydration, abdominal pain, blood, or pale/clay-colored stool. MedlinePlus guidance lists causes including infections, celiac disease, chronic pancreatitis, inflammatory bowel disease, cystic fibrosis, and malabsorption.
If the patient says when he excretes it smells and it looks almost solid but slightly mixes with water and colour change in water to stool colour
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chronic diarrhea stool consistency
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Bristol stool chart loose stools when to seek medical care official health
That description sounds like a soft to mushy, partly formed stool, rather than fully watery diarrhea. On the Bristol Stool Scale, it is often closest to:
- Type 5: soft blobs with clear edges, or
- Type 6: mushy stool with ragged edges.
A stool that looks nearly solid but partly disperses in toilet water, making the water brown, can be normal. Stool pigment and small soft particles commonly mix with the water. This alone does not prove infection, malabsorption, or bleeding.
The smell also varies with diet, bowel bacteria, and how long stool remains in the intestine. It becomes more concerning if it is persistently very foul and accompanied by:
- Frequent loose stools, especially more than 3/day
- Abdominal pain, fever, vomiting, bloating, or excess gas
- Blood, mucus, black-tarry stool, or pale/clay-colored stool
- Greasy, floating, bulky stool that is difficult to flush
- Weight loss or poor appetite
- Symptoms lasting more than 1-2 weeks
If there are no warning symptoms and this is occasional, advise adequate fluids and review recent food changes, antibiotics, dairy intolerance, or gastrointestinal upset. Persistently foul, loose stool with bloating and weight loss needs clinical evaluation, potentially including stool examination for infection or fat/parasites. MedlinePlus guidance lists diet changes as common, but also notes infections and malabsorption-related illnesses as possible causes.
What stool changes should prompt urgent medical care?
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acute diarrhea AND red flags
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adult diarrhea emergency warning signs blood black stools dehydration official health
Seek urgent medical care today if stool changes include any of the following:
| Warning sign | Why it matters |
|---|---|
| Black, tarry, sticky stool | May indicate bleeding higher in the stomach or intestine |
| Bright-red blood, maroon stool, or blood clots | Possible intestinal bleeding |
| Pus or large amounts of mucus with diarrhea | May indicate a significant intestinal infection or inflammation |
| Severe or worsening abdominal pain, swollen abdomen, or rectal pain | Can indicate serious infection, obstruction, appendicitis, ischemia, or inflammation |
| Frequent vomiting or inability to keep fluids down | Risk of rapid dehydration |
| Dehydration signs: very dry mouth, extreme thirst, dizziness/fainting, confusion, very dark urine, or much less urine | May require urgent fluid replacement |
| High fever, chills, marked weakness, or confusion | Possible serious infection |
| Six or more loose stools in 24 hours, especially with weakness or dehydration | High fluid and electrolyte loss |
| Persistent diarrhea for more than 2 days in adults | Needs assessment, especially if worsening |
| Pale/clay-colored stools, especially with yellow eyes/skin or dark urine | May suggest impaired bile flow or liver/biliary disease |
| Greasy, bulky, floating, very foul-smelling stools plus weight loss | Possible fat malabsorption or pancreatic/bowel disease. Arrange prompt medical review |
| New change in bowel habit with unexplained weight loss, anemia, or fatigue | Needs medical evaluation for an underlying bowel disorder |
Go to an emergency department now for black tarry stool, significant fresh blood, fainting/confusion, severe abdominal pain, severe dehydration, or inability to drink fluids.
Infants, young children, older adults, pregnant people, and people with weakened immunity or serious chronic illnesses should seek care earlier because dehydration and infection can become serious faster. The NIDDK diarrhea guidance lists blood or pus in stool, black stool, severe pain, frequent vomiting, altered mental state, and dehydration as reasons for prompt medical help.
How does stool turn black
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melena upper gastrointestinal bleeding
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black stool melena iron bismuth causes official health
Stool turns black mainly for two reasons:
-
Digested blood, called melena
- Bleeding from the food pipe, stomach, or upper small intestine exposes blood to stomach acid and digestive enzymes.
- Hemoglobin is chemically altered as it travels through the gut, making stool jet black, tarry, sticky, and often very foul-smelling.
- Causes include stomach or duodenal ulcers, gastritis, varices, or use of NSAID pain medicines such as ibuprofen, naproxen, and aspirin.
-
Non-bleeding discoloration
- Iron tablets
- Bismuth medicines, such as Pepto-Bismol
- Activated charcoal
- Large amounts of black licorice, blueberries, or blood sausage
Black stool from iron or bismuth is usually formed and not tarry or sticky. They can darken stool without causing bleeding.
Seek emergency care now if black stool is tarry/sticky or occurs with dizziness, fainting, weakness, rapid heartbeat, abdominal pain, vomiting blood, or coffee-ground vomit. A clinician can test the stool for blood. MedlinePlus explains black stool causes.
Now explain me like a professor about alzheimer like a lecture
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Alzheimer disease treatment
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Alzheimer disease brain atrophy hippocampus amyloid plaque tau neurofibrillary tangle pathology diagram
Alzheimer Disease: A Short Clinical Lecture
1. What is Alzheimer disease?
Alzheimer disease is a progressive neurodegenerative brain disorder. It gradually damages neurons, especially those involved in memory, thinking, language, judgment, and everyday functioning.
It is the most common cause of dementia in older adults. Dementia is not one disease. It is a syndrome of decline in cognitive abilities severe enough to affect independent daily life. Alzheimer disease is one important cause of that syndrome.
The core clinical pattern is:
Gradual onset + slowly progressive decline, usually beginning with recent-memory impairment.
For example, a person may repeatedly ask the same question, forget recent conversations or appointments, misplace familiar objects, and later develop trouble managing money, medicines, travel, language, and self-care.
2. Normal ageing versus Alzheimer disease
Occasional forgetfulness is common with normal ageing. Alzheimer disease is suspected when memory difficulty is progressive and disrupts normal life.
| Normal ageing | Suggestive of Alzheimer disease |
|---|---|
| Occasionally forgets a name but remembers it later | Repeatedly forgets recent conversations or events |
| Misplaces an item occasionally | Puts items in unusual places and cannot retrace steps |
| Takes longer to learn a new task | Cannot manage a familiar task, such as cooking or paying bills |
| Sometimes makes an incorrect decision | Persistent poor judgment, unsafe decisions, financial vulnerability |
| Forgets a word occasionally | Increasing word-finding difficulty and impaired conversation |
| Remains independent | Needs help with medicines, finances, meals, hygiene, or navigation |
3. What happens in the brain?
Two abnormal proteins are central to Alzheimer disease:
A. Amyloid-beta plaques
Amyloid-beta is a protein fragment. In Alzheimer disease, it accumulates outside neurons and forms sticky deposits called amyloid plaques.
Think of plaques as abnormal material accumulating between nerve cells. Their presence is associated with disruption of neuronal communication and activation of inflammatory cells in the brain.
B. Tau neurofibrillary tangles
Tau is normally an internal protein that helps stabilize microtubules, the internal transport tracks of neurons.
In Alzheimer disease, tau becomes abnormally phosphorylated, detaches from microtubules, and aggregates inside neurons as neurofibrillary tangles. The neuron then loses its transport system, malfunctions, and eventually dies.
A typical cerebrospinal-fluid biomarker pattern is low beta-amyloid with increased total tau and phosphorylated tau, reflecting amyloid deposition and neuronal injury.
C. Neuronal loss and brain atrophy
The disease often begins in the hippocampus and medial temporal lobe, regions needed for forming new memories. As damage progresses, it spreads to association areas of the cerebral cortex.
This produces:
- Hippocampal and cerebral atrophy
- Enlargement of brain ventricles and sulci on imaging
- Loss of cholinergic neurons, which contributes to memory impairment
A simple sequence is:
Amyloid accumulation -> tau pathology -> synaptic dysfunction -> neuronal death -> brain shrinkage -> worsening cognition and function.
Amyloid is important, but the distribution and amount of tau pathology tend to correlate more closely with symptom severity.
4. Types of Alzheimer disease
Late-onset Alzheimer disease
- Begins after age 65
- Most common form
- Usually multifactorial: age, vascular health, genetic susceptibility, lifestyle, and environment all contribute
Early-onset Alzheimer disease
- Begins before age 65
- Less common
- May have a stronger genetic contribution
- Rare inherited forms can involve pathogenic variants in APP, PSEN1, or PSEN2
APOE gene
The APOE ε4 allele increases risk but does not guarantee that a person will develop Alzheimer disease. Conversely, someone without APOE ε4 can still develop it. APOE testing is therefore not a stand-alone diagnostic test.
5. Clinical stages
Stage 1: Preclinical disease
Brain amyloid and/or tau changes may be present, but the individual has no obvious symptoms.
Stage 2: Mild cognitive impairment due to Alzheimer disease
There is measurable decline, often in recent memory, but the person remains mostly independent in daily activities.
Example: They may need more reminders or make mistakes with complex finances but still dress, eat, travel locally, and perform personal care independently.
Stage 3: Mild dementia
Symptoms interfere with independent living.
Common features:
- Repetition of questions
- Losing objects
- Difficulty with planning, money management, medications, or driving
- Word-finding problems
- Trouble navigating unfamiliar places
- Subtle personality or behavior change
Stage 4: Moderate dementia
There is increasing dependence.
Common features:
- Significant memory loss
- Disorientation to time and place
- Difficulty recognizing familiar people at times
- Agitation, wandering, suspiciousness, hallucinations, sleep disturbance
- Need for help with dressing, bathing, meals, and continence
Stage 5: Severe dementia
The person becomes fully dependent.
Common features:
- Very limited speech and recognition
- Inability to walk independently later in the illness
- Dysphagia, weight loss, aspiration risk
- Urinary and fecal incontinence
- Immobility, infections, pressure injury risk
6. Symptoms beyond memory loss
Alzheimer disease is not only a memory condition. It affects several cognitive domains.
| Domain | Examples of impairment |
|---|---|
| Episodic memory | Forgetting recent events, repeating questions |
| Executive function | Poor planning, unsafe cooking, difficulty managing money |
| Language | Word-finding difficulty, reduced fluency, later impaired comprehension |
| Visuospatial ability | Getting lost, misjudging distances, trouble recognizing objects |
| Attention | Difficulty following a conversation or completing multistep tasks |
| Behavior and mood | Apathy, irritability, depression, anxiety, agitation, suspiciousness |
| Sleep | Day-night reversal, fragmented sleep, nighttime wandering |
7. How is Alzheimer disease diagnosed?
Diagnosis is clinical, supported by cognitive assessment, examination, laboratory studies, and selected biomarkers or imaging.
Step 1: History from patient and informant
A reliable family member or caregiver is important because the patient may not recognize the extent of decline.
Ask about:
- Onset and progression
- Memory, language, behavior, and daily functioning
- Medication use, alcohol or substance use
- Depression and sleep
- Falls, gait changes, urinary symptoms
- Family history
- Impact on finances, cooking, driving, and medicines
Step 2: Cognitive assessment
Common tools include:
- Mini-Mental State Examination, MMSE
- Montreal Cognitive Assessment, MoCA
- Mini-Cog
- Formal neuropsychological testing when needed
These tests support assessment but do not diagnose Alzheimer disease by themselves.
Step 3: Look for reversible or alternative causes
Common initial investigations may include:
- Complete blood count
- Electrolytes, glucose, kidney and liver function
- Thyroid-stimulating hormone
- Vitamin B12, with other tests guided by history
- Depression assessment
- Medication review, especially sedatives, anticholinergic medicines, opioids, and alcohol
Step 4: Brain imaging
CT or MRI is used to exclude structural conditions such as tumor, subdural hematoma, hydrocephalus, or large stroke. MRI may also show hippocampal and medial temporal atrophy.
Step 5: Alzheimer biomarkers, when appropriate
Specialist evaluation may use:
- Amyloid PET
- Tau PET
- Cerebrospinal-fluid amyloid and tau testing
- Selected blood biomarker tests
In the United States, the FDA has cleared a blood test measuring the plasma pTau217/beta-amyloid 1-42 ratio as an aid to diagnosis in symptomatic adults aged 55 or older. It should be interpreted by clinicians within a full diagnostic assessment, not used as a screening test for everyone. FDA blood-test announcement
8. Important conditions that can mimic Alzheimer disease
Before labeling someone as having Alzheimer disease, consider:
- Depression, sometimes called pseudodementia
- Delirium from infection, dehydration, medication effects, or metabolic illness
- Vascular cognitive impairment
- Lewy body dementia
- Frontotemporal dementia
- Normal-pressure hydrocephalus
- Hypothyroidism
- Vitamin B12 deficiency
- Sleep apnea
- Hearing or visual impairment
- Drug-induced cognitive impairment
Delirium is different: it begins suddenly, fluctuates over hours or days, and often includes impaired attention. Alzheimer disease usually develops gradually over months to years.
9. Treatment
There is no complete cure at present, but treatment can support function, reduce symptoms, improve safety, and in selected early cases modestly slow progression.
A. Medicines for cognitive symptoms
| Drug group | Examples | Main role |
|---|---|---|
| Cholinesterase inhibitors | Donepezil, rivastigmine, galantamine | Mild to moderate disease; may give modest symptomatic benefit |
| NMDA receptor antagonist | Memantine | Usually moderate to severe disease; may be combined with a cholinesterase inhibitor |
Cholinesterase inhibitors increase acetylcholine signaling. Common adverse effects include nausea, diarrhea, appetite or weight loss, vivid dreams, slow heart rate, and fainting. Use caution in patients with bradycardia, syncope, or certain conduction disorders.
Memantine modulates glutamate signaling. Possible adverse effects include dizziness, constipation, headache, and confusion.
These medicines are symptomatic treatments. They do not restore dead neurons or cure Alzheimer disease.
B. Anti-amyloid disease-modifying treatments
For carefully selected people with mild cognitive impairment or mild dementia due to confirmed Alzheimer pathology, anti-amyloid monoclonal antibodies may modestly slow cognitive and functional decline.
In the United States, these include:
- Lecanemab
- Donanemab
They require confirmation of brain amyloid pathology and planned MRI monitoring. Important risks include amyloid-related imaging abnormalities (ARIA), which can involve brain swelling or small brain hemorrhages. Risk assessment includes MRI findings, anticoagulant use, and APOE genotype in relevant settings. These drugs are not appropriate for advanced dementia and should be prescribed through a specialist service. Alzheimer’s Association treatment summary
C. Managing behavioral and psychological symptoms
Always first look for a trigger:
- Pain
- Constipation
- Urinary infection or retention
- Sleep deprivation
- Medication adverse effects
- Hunger, thirst, loneliness, overstimulation
- Change of routine or unfamiliar environment
Use non-drug approaches first:
- Calm, simple communication
- Consistent routine
- Adequate light in daytime and quiet at night
- Familiar faces and objects
- Hearing aids and eyeglasses when needed
- Avoid arguing with delusions. Reassure and redirect.
- Exercise and meaningful activity
Sedating medicines and antipsychotics are not routine first-line treatments. They can increase falls, stroke risk, and adverse effects, especially in older adults.
10. Caregiver and safety management
Good Alzheimer care involves the patient, family, caregivers, nurses, physicians, social workers, and occupational therapists.
Key areas include:
- Medication supervision
- Financial protection against errors and exploitation
- Driving assessment, with earlier cessation if unsafe
- Fall prevention and home safety
- Identification bracelet or location plan for wandering risk
- Nutrition, hydration, oral health, and constipation prevention
- Advance care planning while the person can participate in decisions
- Caregiver support and respite care
The aim is not just to treat memory loss. It is to preserve dignity, comfort, safety, relationships, and quality of life.
11. Risk reduction
No measure guarantees prevention, but several actions support brain and vascular health:
- Control blood pressure, diabetes, and cholesterol
- Do not smoke
- Regular physical activity
- Treat hearing loss
- Maintain social and cognitive activity
- Adequate sleep and treatment of sleep apnea if present
- Balanced dietary pattern, such as Mediterranean-style eating
- Limit excess alcohol
- Manage depression and isolation
12. Key take-home points
- Alzheimer disease is a progressive neurodegenerative disorder and the leading cause of dementia.
- Early disease usually presents with impaired recent memory, followed by deficits in language, planning, orientation, and daily function.
- Its central pathology involves extracellular amyloid plaques and intracellular tau tangles.
- Diagnosis requires history, functional assessment, cognitive testing, examination, exclusion of reversible causes, and sometimes biomarkers.
- Donepezil, rivastigmine, galantamine, and memantine may offer symptomatic benefit.
- Lecanemab and donanemab may modestly slow decline in selected early, biomarker-confirmed cases but require specialist assessment and MRI safety monitoring.
- Safety measures, caregiver education, behavioral strategies, and advance planning are as important as medication.
If a person has new confusion over hours to days, fever, altered alertness, severe headache, weakness on one side, speech difficulty, or a sudden major change in behavior, treat it as possible delirium or stroke rather than assuming Alzheimer disease and seek urgent assessment.
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