Your 1 Minute Physiology

Fast physiology & pharmacology cheats

1) Insulin & sugar

What → Insulin (from pancreatic β-cells)
How → Glucose into β-cell → ATP rises → K⁺(ATP) channels close → cell depolarizes → Ca²⁺ influx → insulin release. Insulin then causes GLUT4 to move to the membrane in muscle/adipose and activates enzymes for glycogen & fat synthesis.
Effect → Lowers blood glucose, stores fuel as glycogen/fat, inhibits lipolysis.
Clinical note → Rapid effect on glucose uptake in muscle; deficiency → hyperglycemia.

2) Glucagon — the opposite of insulin

How → Activates hepatic GPCR → increases cAMP → activates PKA → promotes glycogenolysis & gluconeogenesis.
Effect → Raises blood glucose quickly (liver fuel release).

3) Caffeine & adenosine

How → Antagonizes adenosine A₁/A₂A receptors (and at high doses inhibits phosphodiesterase) → increased neuronal firing and cAMP.
Effect → Alertness, reduced sleepiness, ↑heart rate, mild diuresis, ↑catecholamines.
Clinical note → Blocks adenosine’s “calm down” signal.

4) Nicotine & acetylcholine receptors

How → Agonist at nicotinic ACh receptors → stimulates CNS & sympathetic ganglia → dopamine release in reward pathway.
Effect → Alertness, addiction, ↑HR/BP, appetite suppression.

5) Alcohol (ethanol)

How → Potentiates GABAA (inhibitory) and inhibits NMDA (excitatory) receptors; also reduces ADH release.
Effect → Sedation, memory impairment, disinhibition, increased urination.
Clinical note → Chronic use causes tolerance, liver changes, nutritional deficiencies.

6) Opioids (e.g., morphine)

How → Mu receptor agonist → opens K⁺ channels, closes Ca²⁺ channels → decreased neuronal firing and neurotransmitter release; lowers cAMP long-term.
Effect → Powerful analgesia, euphoria, respiratory depression, constipation.
Clinical note → Risk of tolerance and dependence.

7) Benzodiazepines

How → Positive allosteric modulators of GABAA → increase frequency of Cl⁻ channel opening.
Effect → Anxiolytic, sedative, anticonvulsant, muscle relaxant.

8) Beta-blockers (quick correction of a common myth)

How → Block β-adrenergic receptors (β1 in heart, β2 in lung/vasculature).
Effect → ↓Heart rate/contractility and blunt sympathetic signs (tremor, tachycardia).
Clinical note → They do NOT help hyperglycemia. Nonselective β-blockers can impair glycogenolysis and mask hypoglycemia symptoms — so they can worsen or hide low glucose, not treat high glucose.

9) Adrenaline / Noradrenaline (epinephrine / norepinephrine)

How → Activate α and β receptors → widespread sympathetic activation.
Effect → ↑HR, vasoconstriction (α), bronchodilation (β2), glycogenolysis, lipolysis, pupil dilation — fight/flight.

10) Cortisol (stress hormone)

How → Nuclear receptor → alters gene transcription → increases gluconeogenesis, protein catabolism, and lipolysis.
Effect → Raises blood glucose long-term, suppresses immunity, maintains blood pressure.

11) ACE inhibitors & ARBs

How → ACE inhibitors block conversion of Ang I → Ang II; ARBs block angiotensin II receptor.
Effect → Vasodilation, decreased aldosterone → lower BP, reduced remodeling of heart/kidney.
Note → ACE inhibitors increase bradykinin (can cause cough).

12) Aspirin (low dose) vs NSAIDs

How → Aspirin irreversibly inhibits COX-1/2 (platelet COX permanently inhibited). Other NSAIDs reversibly inhibit COX.
Effect → Aspirin reduces platelet aggregation (anti-thrombotic); NSAIDs reduce pain/inflammation.

13) Metformin (T2DM staple)

How → Lowers hepatic gluconeogenesis (partly via AMPK activation).
Effect → Lowers fasting glucose, minimal hypoglycemia risk.
Clinical note → First-line for type 2 diabetes.

14) Sulfonylureas (e.g., glipizide)

How → Close pancreatic β-cell KATP channels → depolarize → ↑insulin release.
Effect → Lower blood glucose but risk hypoglycemia.

15) Statins

How → Inhibit HMG-CoA reductase → reduce cholesterol synthesis → upregulate LDL receptors.
Effect → Lower LDL cholesterol, reduce cardiovascular events.

16) SSRIs (selective serotonin reuptake inhibitors)

How → Block serotonin transporter → increases serotonin in synaptic cleft.
Effect → Antidepressant and anxiolytic effects after weeks.

17) How skeletal muscle & fat take up glucose (GLUTs)

How → GLUT4 is insulin-regulated: insulin → PI3K/Akt pathway → GLUT4 moves to membrane → glucose entry. Other tissues (brain) use GLUT1/3 which are insulin-independent.
Effect → Insulin critical for post-prandial glucose disposal into muscle/fat.

18) Pre-ejaculate (“pre-cum”) — what it is and does

How → Secreted by bulbourethral (Cowper’s) glands during sexual arousal; alkaline mucus that lubricates and neutralizes urine acidity.
Effect → Lubrication and neutralization. May contain sperm (from earlier ejaculations left in urethra) — so it can rarely cause pregnancy; it’s not reliable contraception.

19) Diuretics — loop vs thiazide vs K-sparing

How →

• Loop (furosemide): block NKCC in thick ascending limb → strong natriuresis.

• Thiazide: block NaCl cotransporter in distal tubule → moderate diuresis + reduce Ca excretion.

• K-sparing (spironolactone): antagonize aldosterone or block ENaC → conserve K⁺.
  Effect → Remove fluid, lower BP; different electrolytes affected.

20) Insulin sensitizers — TZDs (pioglitazone)

How → PPAR-γ agonists → change gene expression to increase adipocyte insulin sensitivity and decrease free fatty acids.
Effect → Improve glucose control but can cause weight gain/edema.

21) Platelet activation / clotting quick logic

How → Vessel injury → platelet adhesion → aggregation (ADP, thromboxane A2) → coagulation cascade → fibrin mesh.
Effect → Hemostasis; drugs interrupt different steps (aspirin blocks TXA2, P2Y12 inhibitors block ADP receptor, anticoagulants block clotting cascade).

22) How local anesthetic works (lidocaine)

How → Block voltage-gated Na⁺ channels in nerves → prevent action potential propagation.
Effect → Local loss of sensation/pain.

23) Histamine & allergic reactions

How → Mast cell degranulation → histamine binds H1/H2 → vasodilation, bronchoconstriction, gastric acid increase.
Effect → Itching, hives, bronchospasm; antihistamines (H1 blockers) reduce symptoms.

24) Insulin & lipids (quick)

How → Insulin activates lipoprotein lipase and inhibits hormone-sensitive lipase.
Effect → Promotes triglyceride storage; lack of insulin → increased lipolysis → free fatty acids → ketogenesis.

25) How vaccines “teach” immunity quickly

How → Present antigen → activate B and T cells → form memory cells and antibodies.
Effect → Faster, stronger response on future exposure.

26) Anticholinergics (e.g., atropine)

How → Block muscarinic ACh receptors → reduce parasympathetic tone.
Effect → ↑HR, dry mouth, dilated pupils, urinary retention.

27) How benzodiazepines vs barbiturates differ (safety note)

How → Both enhance GABA, but barbiturates increase duration of Cl⁻ channel opening and can directly activate GABA receptors at high doses.
Effect → Barbiturates have a narrower safety margin; benzodiazepines are safer in overdose (unless combined with other depressants).

28) How aspirin may help a heart attack

How → Irreversibly inhibits platelet COX → reduces thromboxane A2 production → less platelet aggregation.
Effect → Reduces clot growth during MI — chewable aspirin recommended acutely (per protocols).

Want this as a printable 1-page cheat sheet?

I can format these into a clean single-page PDF or table (short lines, bold keywords) for clinical review or study. Say “Make printable cheat sheet” and I’ll produce it.

If you want more entries (e.g., hormones, more drugs, immune system quick hacks), tell me which area and I’ll expand.