Vital Signs & Endocrine Disorders
Start with the normal values you must know cold, then work through the hormone disorders -- too little ADH, too much ADH, and too much cortisol.
Normal Vital Sign Ranges
These are baseline values. Every abnormal finding in this module is judged against them.
| Vital Sign | Normal Range |
|---|---|
| Temperature | 97-99°F |
| Pulse | 60-100 beats/minute |
| Respirations | 12-20 breaths/minute |
| Blood Pressure | 120/80 mmHg |
Why this matters: Cushing's triad (later in this guide) is defined entirely by vital signs going the "wrong" direction -- a slow pulse, a high blood pressure, and a slow/irregular respiratory rate. You cannot recognize it unless you know normal first.
Diabetes Insipidus (DI)
- What it is: A deficiency in -- or resistance to -- antidiuretic hormone (ADH).
- Result: The kidney cannot reabsorb water, so the patient excretes large amounts of dilute urine.
- Signs & symptoms: Frequent urination (polyuria), intense thirst (polydipsia), dry skin, dehydration.
- Despite the name, DI has nothing to do with blood sugar -- it is a water problem, not a glucose problem.
Think: "Always Drinking, Always Dry." No ADH means water pours straight out. The patient drinks constantly and still runs dry.
Syndrome of Inappropriate Antidiuretic Hormone (SIADH)
- Pathology: Excessive ADH released despite a low plasma osmolarity -- the body holds onto water it does not need.
- Common triggers: Lung conditions (especially lung cancer), CNS disorders, and medications such as SSRIs.
- Signs & symptoms: Fluid retention, hyponatremia (dilutional low sodium), headache, nausea, confusion.
- Treatment: Fluid restriction, salt supplementation, and careful diuretic use to correct the hyponatremia.
Remember: "Swollen with Water, Salt Washed Away." Water is retained, so sodium is diluted -- the patient looks puffy and the serum sodium falls.
The confusion, headache, and nausea in SIADH are not from the ADH itself -- they are from hyponatremia. Low sodium pulls water into brain cells, causing cerebral edema. That is why treatment centers on fluid restriction rather than "fixing" the hormone.
DI vs. SIADH -- Mirror Images
These two conditions are opposites. If you learn one, you get the other for free.
Diabetes Insipidus (too little ADH)
- Urine output: high, very dilute
- Fluid status: dehydrated
- Serum sodium: high (concentrated)
- Patient looks: dry skin, thirsty
- Motto: "Always Drinking, Always Dry"
SIADH (too much ADH)
- Urine output: low, concentrated
- Fluid status: fluid overloaded
- Serum sodium: low (hyponatremia)
- Patient looks: swollen, confused
- Motto: "Swollen with Water, Salt Washed Away"
Anchor on ADH. ADH = "anti-diuretic" = hold water. Not enough ADH (DI) means you dump water and dry out. Too much ADH (SIADH) means you hoard water and dilute your sodium. Every other finding follows from that one sentence.
Cushing Syndrome
- Pathology: Excessive cortisol.
- Causes: Pituitary adenomas (when a pituitary adenoma is the cause it is called Cushing's disease), adrenal tumors, or ectopic ACTH production.
- Signs & symptoms: Weight gain with moon face and buffalo hump, hirsutism, skin changes (thin skin, striae, easy bruising), high blood sugar, anxiety and agitation.
Motto: "Excess is the Norm." Too much of everything -- too much fat centrally, too much hair, too much glucose, too much anxiety.
Shortcut: TOO MANY STEROIDS! Cortisol is the body's own steroid. Picture a patient on long-term high-dose prednisone -- that is exactly what Cushing syndrome looks like.
Do not mix these up: Cushing syndrome = excess cortisol (endocrine). Cushing's triad = bradycardia + hypertension + irregular respirations (a neurologic sign of increased intracranial pressure). Same name, completely different topic -- see the Neurologic tab.
Mnemonic Flip Cards
Click each card to reveal the condition it belongs to:
A 45-year-old presents with central weight gain, a rounded "moon" face, a fat pad between the shoulders, new facial hair, thin bruised skin, and a fasting glucose of 168 mg/dL. Which hormone is in excess, and what are three possible sources?
- ADH (also called vasopressin) is made in the hypothalamus and released from the posterior pituitary.
- It acts on the collecting ducts of the kidney, making them permeable to water so water is pulled back into the bloodstream.
- Normal trigger for release: rising serum osmolarity (blood too concentrated) or falling blood volume.
- In SIADH the release is "inappropriate" because it continues even when serum osmolarity is already low.
- Central DI = the pituitary does not make enough ADH. Nephrogenic DI = the kidney does not respond to the ADH that is present.
Diabetes Mellitus
Type 1, Type 2, and gestational diabetes -- plus the classic symptom triad and the numbers used to diagnose them.
Type 1 Diabetes Mellitus
- Pathology: An autoimmune disorder in which the immune system attacks the pancreatic beta cells, leading to no insulin production.
- Typical onset: Childhood or adolescence.
- Signs & symptoms (sudden onset): Frequent urination, increased thirst, extreme hunger, unexplained weight loss, fatigue, irritability.
- Diagnosis: Blood tests showing high glucose with low to no insulin production. Autoantibodies may be present, confirming the autoimmune cause.
Think: "Sudden Storm." Type 1 arrives fast and hits hard -- often a young patient who was fine last month.
Type 2 Diabetes Mellitus
- Pathology: Insulin resistance first, and eventually insufficient insulin production.
- Associated with: Obesity, poor diet, and lack of exercise.
- Signs & symptoms (gradual onset): Similar to Type 1 but milder at first, often with slow-healing wounds, frequent infections, and areas of darkened skin (acanthosis nigricans).
- Diagnosis: Elevated blood glucose on multiple occasions, HbA1c ≥ 6.5%, and often features of metabolic syndrome.
- Treatment: Lifestyle interventions (diet and exercise), oral medications (metformin initially), and possibly insulin therapy as the disease progresses.
Think: "Creeping Concerns." Type 2 sneaks up over years. Many patients are diagnosed only after a wound will not heal or a routine lab comes back high.
Type 1 vs. Type 2 at a Glance
| Feature | Type 1 | Type 2 |
|---|---|---|
| Underlying problem | Autoimmune destruction of beta cells → no insulin | Insulin resistance → later, insufficient insulin |
| Onset | Sudden ("Sudden Storm") | Gradual ("Creeping Concerns") |
| Typical age | Childhood / adolescence | Adulthood, increasingly younger |
| Body habitus | Often thin; unexplained weight loss | Commonly associated with obesity |
| Distinctive findings | Autoantibodies present; low/absent insulin | Slow-healing wounds, frequent infections, darkened skin |
| Treatment | Insulin -- required from diagnosis | Lifestyle, metformin, insulin later if needed |
Exam Tip: The single cleanest distinguisher is the mechanism. Type 1 = the pancreas cannot make insulin. Type 2 = the body cannot use the insulin it makes. Age and weight are supporting clues, not the definition.
Diagnostic Criteria for Prediabetes and Diabetes
Four different tests can establish the diagnosis. Know the cutoffs.
| Test | Prediabetes | Diabetes |
|---|---|---|
| A1C | 5.7-6.4% (39-47 mmol/mol) | ≥ 6.5% (≥ 48 mmol/mol) |
| Fasting plasma glucose | 100-125 mg/dL (5.6-6.9 mmol/L) | ≥ 126 mg/dL (≥ 7.0 mmol/L) |
| 2-hour glucose during a 75-g oral glucose tolerance test | 140-199 mg/dL (7.8-11.0 mmol/L) | ≥ 200 mg/dL (≥ 11.1 mmol/L) |
| Random glucose with classic hyperglycemia symptoms / hyperglycemic crisis | — | ≥ 200 mg/dL (≥ 11.1 mmol/L) |
Notice that 200 mg/dL appears twice -- as the 2-hour OGTT cutoff and as the random glucose cutoff. And 126 mg/dL is the fasting number. If you only memorize three numbers, memorize 6.5% — 126 — 200.
Polydipsia and the Classic Triad
- Polydipsia = excessive thirst and fluid intake. It is a hallmark symptom of diabetes mellitus in both Type 1 and Type 2.
- Polyuria (frequent urination) is closely tied to polydipsia -- increased fluid intake leads to more frequent urination.
- Polyphagia = increased appetite.
The classic triad -- the "3 P's":
- Polydipsia -- excessive thirst
- Polyuria -- excessive urination
- Polyphagia -- excessive hunger
Polydipsia, polyuria, and polyphagia together form the classic triad of diabetes symptoms. Recognizing them early leads to prompt diagnosis and management, preventing complications.
Gestational Diabetes Mellitus (GDM)
- What it is: Impaired glucose tolerance during pregnancy that most commonly develops during the second and third trimesters.
- Possible consequences:
- Hypoglycemia in the newborn
- Large-for-gestational-age infants (macrosomia)
- Fetal defects
- Premature delivery
Why newborn hypoglycemia? The mother's high glucose crosses the placenta, so the fetus makes extra insulin to handle it. At delivery the maternal glucose supply is cut off, but the newborn's insulin level is still high -- so blood sugar crashes.
A 54-year-old with a BMI of 34 comes in for a foot ulcer that has not healed in six weeks. He also mentions recurrent skin infections and dark, velvety patches on the back of his neck. Fasting glucose is 141 mg/dL and A1C is 7.8%. What is the diagnosis and what is the first-line pharmacologic treatment?
Two patients both report drinking water constantly and urinating large volumes. Patient A has a serum glucose of 385 mg/dL. Patient B has a serum glucose of 92 mg/dL but very dilute urine. What condition does each patient most likely have?
- Glucose in the blood attaches to hemoglobin inside red blood cells. The higher the glucose, the more hemoglobin gets coated.
- Red blood cells live about 120 days, so the A1C reflects the average blood glucose over roughly the past 2-3 months.
- This is why A1C cannot be "fixed" by fasting the morning of the test -- unlike a fasting glucose.
- It is used both to diagnose diabetes (≥ 6.5%) and to monitor how well treatment is working over time.
Neurologic Conditions
Increased intracranial pressure, strokes and TIAs, demyelination, headaches, and Parkinson's disease.
Cushing's Triad
Cushing's triad is a clinical constellation of signs that indicates increased intracranial pressure (ICP). The three signs are:
- Bradycardia -- slow heart rate
- Hypertension -- specifically a rising systolic pressure with a widening pulse pressure
- Bradypnea or irregular respirations
Compare to normal vitals: Pulse 60-100, BP 120/80, respirations 12-20. In Cushing's triad the pulse and respiratory rate fall below normal while the blood pressure climbs above it. Two down, one up.
Cushing's triad is a late and ominous sign of increased ICP -- it signals impending brain herniation. Do not confuse it with Cushing syndrome (excess cortisol). If a question gives you a head-injured patient whose heart rate is dropping while blood pressure rises, that is Cushing's triad, and it is an emergency.
Transient Ischemic Attack (TIA)
- Definition: Temporary, focal cerebral ischemia producing reversible neurological deficits without acute infarction -- imaging shows no signs of infarction.
- Often called a "mini-stroke."
- Cause: A temporary blockage of blood flow to the brain, typically from a blood clot or narrowing of the arteries.
- Symptoms: Similar to a stroke, but transient -- usually lasting only a few minutes and resolving within 24 hours.
The defining feature of a TIA is not how long it lasts -- it is that imaging shows no infarction. The tissue was starved but never died. A TIA is a warning shot: it identifies a patient at high risk for a full stroke soon.
Ischemic Penumbra
- The perimeter around the core ischemic area is called the ischemic penumbra.
- In the penumbra, brain cells are still alive but at risk of dying if blood flow is not restored quickly.
- The core is tissue that is already destined to die; the penumbra is the salvageable zone.
Why "time is brain": Every treatment for acute ischemic stroke exists to rescue the penumbra. Restore perfusion fast and that tissue survives; delay and the penumbra is absorbed into the infarct core.
Hemorrhagic Stroke
- What it is: A blood vessel in the brain ruptures and bleeds, leading to the formation of a hematoma.
- Risk factors: Uncontrolled hypertension, age, previous brain aneurysm.
- Symptoms: Left-sided paralysis (hemiplegia), slurred speech (dysarthria), loss of gag reflex, and facial droop -- classic signs of a stroke affecting the right side of the brain.
- CT scan: The presence of a hematoma on CT confirms that the stroke is hemorrhagic in nature.
Remember the crossover: Motor pathways cross in the brainstem, so a right-brain stroke causes left-sided deficits, and vice versa. The side of the body that is weak is the opposite of the side of the brain that is damaged.
The CT scan is what separates the two stroke types, and that distinction changes everything about treatment. Ischemic = blockage of an artery; clot-dissolving therapy may be appropriate. Hemorrhagic = artery leaks into brain tissue and a hematoma is visible on CT; clot-dissolving therapy would be catastrophic.
Ischemic vs. Hemorrhagic Stroke
Ischemic Stroke
- Blockage of an artery
- Brain tissue deprived of oxygen-rich blood
- Produces a core plus a salvageable penumbra
- CT: no hematoma
- Related: TIA is the temporary, reversible version
Hemorrhagic Stroke
- Artery ruptures and leaks into brain tissue
- Forms a hematoma
- Risk factors: uncontrolled HTN, age, prior aneurysm
- CT: hematoma present -- confirms the diagnosis
- Bleeding raises ICP; watch for Cushing's triad
Multiple Sclerosis (MS)
- What it is: An autoimmune disease in which the body's T cells mistakenly attack the myelin sheath -- the protective covering around nerve fibers.
- Location: The central nervous system only -- brain and spinal cord.
- Damaged myelin slows or blocks nerve signal conduction, which is why symptoms are so varied (vision changes, weakness, numbness, coordination problems, fatigue).
Three things to lock in for MS: (1) It is autoimmune. (2) T cells are the attackers. (3) The target is the myelin sheath in the CNS -- not the peripheral nerves.
Trigeminal Autonomic Cephalgia (TAC)
TACs are a group of headache disorders characterized by:
- Excruciating unilateral (one-sided) pain
- Restlessness
- Bloodshot eyes
- Pupil constriction
- Tearing (lacrimation)
- Nasal discharge (rhinorrhea)
The word "autonomic" is the key. The red eye, tearing, runny nose, and constricted pupil are all autonomic nervous system symptoms on the same side as the pain. Cluster headache is the classic TAC -- and autonomic symptoms are exactly what tension headaches lack.
Headache Comparison
| Migraine | Tension | Cluster | |
|---|---|---|---|
| Character | Unilateral; throbbing, hammering | Bilateral; dull, "band-like" compression | Unilateral; piercing, stabbing, burning |
| Course | Slowly progressing; may last up to 72 hours | Initially episodic; may progress to chronic daily headaches | Clustering of attacks over weeks followed by remission (75% of cases) |
| Additional symptoms | Nausea/vomiting, photophobia/phonophobia, aura may occur | Photophobia/phonophobia may occur; no nausea, no vomiting | Autonomic symptoms (lacrimation, rhinorrhea, sweating) |
| Demographics | Women > men; onset 15-25 years; exercise exacerbates | Women > men; onset 30-40 years; exertion does not exacerbate | Men > women; onset 20-40 years; attacks often at night; short attacks (30-40 min) |
| Remember | High risk of medication-overuse headache | Autonomic symptoms are absent | The classic trigeminal autonomic cephalgia |
Parkinson's Disease
- What it is: A chronic, progressive neurodegenerative disorder resulting from the gradual degeneration and death of dopaminergic neurons in the substantia nigra.
- The substantia nigra produces dopamine, the neurotransmitter that regulates movement, coordination, and balance.
- Losing those neurons means losing dopamine -- and with it, smooth controlled movement.
One sentence to remember: Parkinson's = dopamine down, because the substantia nigra is dying.
A 68-year-old with uncontrolled hypertension suddenly develops left-sided paralysis, slurred speech, loss of gag reflex, and facial droop. CT shows a hematoma. Which side of the brain is affected, and what type of stroke is this?
A patient has 20 minutes of right arm weakness and slurred speech that fully resolves. She arrives at the ER two hours later with a completely normal neurologic exam, and imaging shows no infarction. What happened, and why does it still matter?
- The skull is a closed box. Bleeding or swelling inside it raises pressure with nowhere to expand.
- Rising ICP squeezes cerebral arteries, so the body raises systemic blood pressure to keep pushing blood into the brain -- that is the hypertension.
- Baroreceptors sense the high pressure and reflexively slow the heart -- that is the bradycardia.
- As pressure compresses the brainstem, the respiratory center falters -- that is the bradypnea or irregular respirations.
- Because the brainstem is already being compressed by the time all three appear, Cushing's triad is a late finding and signals impending herniation.
Renal & Urinary Disorders
Glomerular damage, kidney infection, stones, obstruction, and incontinence -- organized from the glomerulus outward.
Nephrotic Syndrome
- What it is: A condition where the glomerulus is damaged and proteins leak out of the bloodstream into the urine.
- The protein that leaks out is mostly albumin, which leads to hypoalbuminemia and decreased colloid oncotic pressure -- which in turn causes edema.
- The three symptoms: hypoalbuminemia, proteinuria, and edema.
- Recovery is indicated by a reduction or disappearance of proteinuria.
Why albumin causes swelling: Albumin is the protein that holds fluid inside blood vessels by generating colloid oncotic pressure -- think of it as the sponge that keeps water in the bloodstream. Lose albumin into the urine and fluid leaks into the tissues. That is the edema.
If a question asks how to tell whether a patient with nephrotic syndrome is recovering, the answer is a reduction or disappearance of proteinuria. The protein in the urine is the direct marker of glomerular leakage -- when it falls, the glomerulus is healing.
Glomerulonephritis
- What it is: Inflammation of the glomeruli that affects both kidneys; can be acute or chronic.
- Post-streptococcal glomerulonephritis (PSGN) is the most common type of acute glomerulonephritis.
- It occurs as a complication of a streptococcal infection, typically strep throat.
- The immune system's response to the bacteria leads to inflammation and damage of the glomeruli.
Classic Presentation
- Puffiness of the eyelids (periorbital area) and facial edema
- Dark, cola-colored urine because it contains RBCs
- Elevated blood pressure
- CVA tenderness (costovertebral angle tenderness) on exam
PSGN is not the strep bacteria attacking the kidney directly -- it is the immune complexes formed against strep that deposit in the glomeruli and trigger inflammation. That is why it shows up a week or two after the sore throat, not during it.
Nephrotic Syndrome vs. Glomerulonephritis
Both involve the glomerulus. What leaks through is what separates them.
Nephrotic Syndrome
- Glomerulus is damaged and leaky
- What leaks: protein (albumin)
- Urine: frothy, heavy proteinuria
- Hallmarks: hypoalbuminemia, proteinuria, edema
- Recovery marker: proteinuria decreases or disappears
Glomerulonephritis (PSGN)
- Glomerulus is inflamed
- What leaks: red blood cells
- Urine: dark, cola-colored (hematuria)
- Hallmarks: periorbital/facial edema, elevated BP, CVA tenderness
- Trigger: recent streptococcal infection (strep throat)
Pyelonephritis (Kidney Infection)
- What it is: An infection of the kidney.
- Classic manifestations: Flank pain, chills, and fever.
- Urinalysis shows: pyuria (elevated white blood cell count in the urine) and bacteriuria (bacteria in the urine).
How Bacteria Reach the Kidney (Ascending Infection)
- Colonization -- bacterial colonization in the periurethral area allows ascension via the urethra
- Uroepithelium penetration -- bacterial fimbriae allow attachment to and penetration of bladder epithelial cells
- Ascension -- sufficient bacterial colonization leads to ascension through the ureters
- Pyelonephritis -- bacterial ascension or hematogenous spread infects the renal parenchyma
- Acute kidney injury (AKI) -- continuous inflammation results in interstitial edema, interstitial nephritis, and ultimately AKI
Location tells you the name: Urethra = urethritis. Bladder = cystitis. Kidney = pyelonephritis. Same ascending bacteria, different level of the tract -- and flank pain plus fever means it has reached the kidney.
Renal Calculi (Kidney Stones)
Risk Factors
- Dehydration: Not drinking enough fluids, especially water, leads to concentrated urine, increasing the risk of minerals crystallizing and forming stones.
- Dietary factors -- high protein intake: A diet high in animal protein can raise uric acid levels, contributing to uric acid stones.
The single best prevention message: increase fluid intake. Dilute urine keeps minerals dissolved; concentrated urine lets them crystallize.
Uropathy and Obstruction
- Uropathy is a broad term for any disease or dysfunction of the urinary tract.
- Obstructive uropathy is a specific type where the flow of urine is obstructed, leading to a backup of urine and potential damage to the kidneys.
Hydronephrosis (Swelling of the Renal Pelvis)
- Hydronephrosis is characterized by dilation of the renal pelvis.
- It is frequently caused by an obstruction within the urinary tract.
Think of it as a chain: an obstruction (often a stone) blocks outflow → urine backs up → the renal pelvis dilates (hydronephrosis) → sustained back-pressure damages kidney tissue. This is exactly the mechanism behind post-renal dysfunction below.
Renal Dysfunction: Pre-renal vs. Post-renal
| Type | Problem | Common Causes |
|---|---|---|
| Pre-renal | Decreased blood flow to the kidneys (reduced renal perfusion) | Hypovolemia (low blood volume) and heart failure (inadequate pumping of blood by the heart) |
| Post-renal | Obstruction of urine flow after it leaves the kidneys | A kidney stone or a tumor blocking the ureters |
Follow the plumbing:
- PRE-renal = the problem is before the kidney -- not enough blood is arriving.
- POST-renal = the problem is after the kidney -- urine cannot get out.
Incontinence
- Functional incontinence: Occurs due to physical or cognitive impairments -- the urinary tract works, but the person cannot reach the toilet in time or does not recognize the need.
- Stress incontinence: Involuntary urine leakage during activities that increase intra-abdominal pressure -- such as squatting, coughing, or lifting -- due to weakened pelvic floor muscles or urethral sphincter.
| Type | What Triggers the Leak | Underlying Problem |
|---|---|---|
| Stress | Coughing, squatting, lifting, sneezing, laughing | Weak pelvic floor muscles or urethral sphincter |
| Functional | Cannot reach or use the toilet in time | Physical or cognitive impairment (not a urinary tract problem) |
| Urge | Sudden, intense need to void | Overactive bladder contractions |
| Overflow | Constant dribbling; bladder never fully empties | Bladder outlet obstruction or poor bladder contraction |
The word in the stem tells you the type. "Leaks when she coughs or lifts her grandchild" = stress. "Has arthritis and a walker and cannot get to the bathroom in time" = functional. Functional incontinence is the one where the bladder itself is fine.
A patient arrives with severe right flank pain, fever of 101.8°F, and chills. Urinalysis shows pyuria and bacteriuria. What is the diagnosis, and how did the bacteria get to the kidney?
A patient with a stone lodged in the right ureter has an ultrasound showing dilation of the right renal pelvis. Name this finding, classify the renal dysfunction, and explain the risk to the kidney.
- Blood vessels constantly push fluid out into tissue (hydrostatic pressure) and pull it back in (oncotic pressure).
- The "pull back in" force comes almost entirely from albumin dissolved in the plasma.
- In nephrotic syndrome, albumin escapes through the damaged glomerulus into the urine.
- With less albumin in the blood, the pull-back force drops -- fluid stays in the tissue.
- That trapped fluid is the edema you see in the face, legs, and abdomen.
- Glomerulus: nephrotic syndrome (protein leaks out), glomerulonephritis/PSGN (inflammation, RBCs leak out).
- Renal parenchyma: pyelonephritis (infection), acute kidney injury.
- Renal pelvis: hydronephrosis (dilation from backed-up urine).
- Ureters: renal calculi lodging and obstructing; tumors compressing.
- Bladder: cystitis; urge and overflow incontinence.
- Urethra / outside the tract entirely: urethritis; stress and functional incontinence.