Exam - Tricky Concepts Flashcards
(70 cards)
1
Q
What are the four types of protein receptors and how do they work?
A
- transmembrane receptor with linked enzymatic domain: ligand bids to receptor in extracellular environment. This triggers dimerisation (binding of two receptors) to activate the enzyme inside the cell. This triggers a cascade of events inside the cell.
- intracellular receptor: small lypophillic molecules diffusion through the plasma membrane and dock with an intracellular receptor. Causes changes to gene expression.
- G-coupled protein receptor: 7 transmembrane domains. Ligand binds to one and triggers a response inside the cell. The linked G-protein activates and causes a cascade of events inside the cell.
- ion channel: ligand binds to receptor, opening it. Ions can pass through the channel.
2
Q
Brief steps of the cell cycle & mitosis.
A
G1: Cell is growing, preparing to divide.
S: DNA replication
G2: Increase in mitosis promoting factor to prepare the cell for mitosis
M: Mitosis:
1. prophase: nuclear envelop fragments, chromatin condenses to chromosomes, mitotic spindle fibres form and attach at the kintechore of each chromosome.
2. metaphase: chromosomes line up along metaphase plate and prepare for contraction.
3. anaphase: Contraction of mitotic spindle fibres and pulling chromatids to opposite poles of the cell.
4. telophase: nuclear enevlop forms around two sets of DNA, cell elongates.
5. cytokensis: cytoplasm splits at the cleavage and two new daughter cells are formed.
3
Q
Describe the process of receptor-mediated endocytosis.
A
- Receptors are triggered by a ligand.
- plasma membrane forms an invagination and clathrin (a protein coats this pit).
- An endosome is formed and transports molecules inside the cell.
- Clathrin leaves the endosome and a primary lysosome binds with the endosome forming a secondary lysosome.
- The lysosome fragments the contents of the vesicles.
- Lysosome exits and same with contents.
- Receptors remain on the endosome and travel back to the plasma membrane to fuse with the plasma membrane and prepare for the same process again.
4
Q
How is H. Pylori degraded?
A
- Via macrophages instead of phagocytic killing.
- H. Pylori has built defence against lysosomal degrading enzymes and therefore a macrophage must engulf it. Can cause GORD and peptic ulcer disease.
5
Q
What is an example of a clinical scenario for cells, tissues, and membranes?
A
Lysosomal storage disease:
- Caused by faulty lysosomes. They are unable to degrade the contents and end up with a big pool of toxic waste.
- This build of toxins can kill tissue and cause major implications.
- Treatments include enzyme replacement therapy whereby recombinant DNA is infused via an IV.
- This enters the cell via receptor mediated endocytosis.
- The enzyme is released from the receptor and can breakdown these molecules.
6
Q
What are the different types of intracellular junctions?
A
- gap junctions:
- connect cells via proteins called connexons. Permit the movement of ions, water, and small molecules throughout the junction. Conduct action potentials. - tight junctions:
- Tightly seal epithelia so that no interstitial fluid can travel to the basement membrane. - desmosomes: cell adhesion molecules connect the cytoskeleton to prevent twisting and shifting of the epithelia. Proteoglycans are involved in maintaining this structure.
- hemidesmosomes:
- protein fibres connect epithelia to the basement membrane.
7
Q
What is the difference between exocrine and endocrine glands?
A
- exocrine glands secrete their product directly to the apical surface of epithelia, commonly transported via ducts.
- endocrine glads secrete hormones into the bloodstream.
8
Q
What are the three types of exocrine glands and how do they secrete their products?
A
- apocrine:
- mammary glands
- secrete milk
- Part of the cell and its associated cytoplasm detaches from the rest of the cell. This is from the apical surface. As it detaches it releases contents. - holocrine:
- the entire cell lyses to release its contents.
- Stem cells closer to the basement membrane continue regeneration.
- sebaceous glands, which release sebum. - merocrine:
- sweat glands.
- release contents via exocytosis.
9
Q
What are the specialised connective tissue proper cells and what are their roles?
A
- fibroblasts: secrete hyaluronan and extracellular protein fibres which make ground substance so viscous.
- fibrocytes: maintain connective tissue proper fibres.
- mesenchymal: Stem cells, regenerate scar tissue.
- adipocytes: stores fat and energy
- melanocytes: store pigment (melanin)
- macrophages: phagocytic cells which engulf and degrade harmful bacteria.
- microphages (neutrophils and eosinophils): phagocytic blood cells which assist macrophages in immune response.
- lymphocytes: immune response.
- mast cells: release histamine during inflammation.
10
Q
What are the three types of connective tissue and their associate subunits?
A
- connective tissue proper:
- loose: areolar, adipose, elastic
- dense: regular, irregular, reticular - supportive connective tissue:
- bone
- cartilage: fibrocartilagonous, hyaline, elastic - fluid connective tissue:
- blood
- lymph
11
Q
What are the three types of fascia?
A
- superficial:
- fat
- adipose tissue and areolar tissue - deep:
- dense, regular connective tissue
- found in join capsules - subserous:
- in between superficial and deep tissue.
- areolar connective tissue.
12
Q
What are the four types of membranes and explain them?
A
- serous:
- lines body cavities, prevents abrasion of internal organs. Different cavities include, pleura of the lungs, pericardium, peritoneal.
- Have a parietal and visceral membrane and secrete a fluid to allow for lubrication and prevent friction in between the two layers.
- simple squamous epithelia and areolar connective tissue - mucous:
- secrete mucous to lubricate the passageway and trap pathogens as a the first line of defence.
- simple columnar epithelium, areolar connective tissue. - cutaneous:
- skin
- waterproof, provides protection, stops things from entering our body that shouldn’t
- stratified squamous epithelium, areolar connective tissue and dense irregular connective tissue. - synovial:
- lines synovial joints
- secretes synovial fluid nourishing hyaline cartilage
- no true epithelium, areolar connective tissue
13
Q
What are two clinical examples of epithelial cell dysfunction?
A
- Asthma:
- can be caused by genetic factors or irritants. In an asthma patient, their airways are constricted because smooth muscle mass is significantly larger, epithelial cells tight junctions have been dismantled, they secrete too much mucous, and the loss of ciliated cells.
- during an asthma attach when the smooth muscle constricts, adrenaline is administered to dilate airways. - Celiac disease:
- autoimmune response to gluten.
- gluten triggers immune response whereby the microvilli of the small intestine is damaged.
- this decreases absorption capacity.
14
Q
What is a clinical example of connective tissue dysfunction?
A
Rehumatoid arthitis:
- autoimmune disease impacting the membrane around joints.
- as a result of inflammation it can damage body systems including the skin, lungs, heart, and blood vessels.
15
Q
What are the specialised neuron cells?
A
- bipolar
- unipolar
- multipolar
- anaxonic
16
Q
What are specialised neuroglia cells?
A
CNS:
- astrocytes: largest and most prominent, protect the blood brain barrier.
- oligodendrocytes: create myelin sheath
- ependymal: produce and monitor cerebrospinal fluid (CSF)
- microglia: phagocytic cells protecting the environment around neurons.
PNS:
- satellite: protect surround PNS environment
- Schwann cells: create myelin sheath
17
Q
Describe the process of how a graded potential is formed.
A
- chemical stimulus opens chemically gated sodium ion channels.
- small influx of sodium ions into the cell due to the electrical gradient.
- Small depolarisation, however it does not reach the -60m/v threshold for the conduction of an action potential.
- therefore, the graded potential is small and localised. - Na+ channel closes and the resting membrane potential of -75 m/v is restored via leak channels and the Na+/K+ exchange pump.
18
Q
Describe how an action potential is formed?
A
- Large chemical stimulus opens chemically-gated sodium ion channels, therefore there is a large influx of sodium into the cell.
- Surpasses -60m/v threshold which triggers voltage-gated sodium ion channels to open.
- Further influx of sodium ions causes depolarisation of the membrane.
- At +30 mv/v, Na+ gates close and voltage gated K+ ion channels open, resulting in a K+ efflux.
- This causes repolerisation.
- At resting membrane potential (-75m/v) K+ channels slowly close, resulting in a brief hyperpolerisation phase.
- Resting membrane potential is restored via leak channels and the sodium/potassium exchange pump.
19
Q
What type of propagation of an action potential occurs on a myelinated axon vs a non-myelinated axon?
A
- myelinated: saltatory propagation
- non-myelinated: continuous propagation
20
Q
Describe how myasthenia gravis occurs?
A
- happens at the neuromuscular junction
- autoimmune disease
- antibodies secreted by differentiated lymphocytes (B-cells) block acetylcholine receptors on the muscle fibre.
- This reduces the amount of neurotransmission that can occur between the neuron and post synaptic cell.
- therefore, there is not enough to trigger the opening of voltage gated calcium channels in the sarcoplasmic reticulum of the muscle fibre.
- therefore no muscle contraction can occur.
- causes muscle weakness.
- first sign is drooping eyelid.
Treatment:
- immunosupressants to reduce the production of harmful antibodies.
21
Q
Describe the Haversian system.
A
- within bone.
- central vein and artery
- osteocyte within lacuna
- canaliculi connect osteocytes to transmit messages.
22
Q
Describe the process of endochondral ossification.
A
- cartilage formation: STEM cells differentiate into chondrocytes and proliferate to form a cartilage long bone structure.
- cartilage growth: chondrocytes grow and their cells expand, however they grow too large and lyse, expelling their contents onto the cartilage matrix. This alters the pH and prompts arteries and nutrients to come and form a primary ossification centre.
- primary ossification centre: nutrient artery comes and provides the nutrients for osteoblast activity. Osteoblasts create a collagen fibre matrix with hydroxyapatite crystals for increased bone strength.
- medullary cavity: the bone is reshaped to form a medullary cavity.
- secondary ossification centre: the arteries migrate to the epiphyses to form a secondary ossification centre. Spongy bone is formed by osteoblasts.
- formation of cartilage on joints: the cartilage on the external edge of the epiphyses where bones articulate remain as hyaline cartilage for optimum bone articulation.
23
Q
Describe long bone growth.
A
- Happens along the epiphyseal plate.
- chondrocyte activity increases on the epiphyseal side of the plate. Osteoblast activity increases on the diaphysis side of the plate.
- between the ages of 18 and 25 cartilage cells stop proliferating and only osteoblast activity keeps occurring, mineralising the cartilage.
- what is left is an epiphyseal line.
24
Q
Describe flat bone formation and growth.
A
Intramembranous ossification:
1. Two plates opposite each other.
2. mesenchymal cells proliferate and differentiate into osteogenic cells. osteogenic cells differentiate into osteoblast.
2. Osteoblasts begin bone formation, growing the two plates toward each other.
25
What is the bodies response to low levels of blood calcium?
- Stimulate parathyroid gland to secrete parathyroid hormone.
PTH:
- increases bone resportion, increases calcium absorption at the kidneys and increases secretion of calcitriol (vitamin D) to increase absorption of calcium in the digestive tract.
26
What is the bodies response to high levels of blood calcium?
- Thyroid gland increases secretion of calcitonin.
Calcitonin:
- increases filtration of calcium at kidneys
- increases bone formation.
27
Difference between fast vs slow muscle twitches.
Fast:
- increased number of myofibrils
- decreased number of mitochondria
Slow:
- increased number of mitochondria
- more myoglobin
- decreased number of myofibrils
28
Effect of exercise on muscle.
- 2 ways
Endurance:
- increased number of mitochondria
- increased size of mitochondria
- increased arteries (more O2 available)
- increased myoglobin
Strength:
- increased number of myofibrils
- increased size of muscle fibres
- increased neural activity because of more neuromuscular junctions
29
Describe Wolf's Law.
- compression force vs tensile force
- compression force = more bone formation
- tensile force = more bone resorption
30
Describe two clinical examples of issues with bones.
Osteoporosis:
- increased osteoclast activity therefore increased bone resorption
- forms more holes in spongy bone, decreasing bone density
- increases the amount of fat and bone marrow instead of bone
- increased risk of fracture
- typically in older people and women
treatments: increase dietary vitamin D and calcium, supplements, sometimes surgery to repair fractures.
Osteomalacia/rickets:
- when bone is soft and moulds to different forces more easily.
- decreased bone strength
- reduced bone mineralisation due to calcium and phosphate deficiencies
treatments: increase intake of these minerals
31
Describe the process of hemostasis.
- blood clotting, three phases, vascular phase, platelet phase, and coagulation phase.
1. Blood vessel is cut.
2. Vascular phase: blood vessel vasoconstricts and forms sticky ends. chemicals to send clotting signals are sent.
3. Platelet phase: platelets are activated and they travel to the site. They stick to the walls of the blood vessels and form a positive feedback loop as they continue signalling clotting compounds to come to the site. The form a clot until inhibitory factors stop the clot.
4. Coagulation phase: The platelets are deactivated but a web needs to be formed around them to secure it in place. Prothromibanse causes the following reaction below. This secrets fibrin which pulls the platelets together and secures the clot.
prothrombin ----> thrombin |
fibrogen -----------------> fibrin
32
What is the histology of the heart?
- Pericardium - overall
- Partietal pericardium
- epicardium (visceral pericardium)
- myocardium - thickest layer of cardiac muscle. Made of muscle fibres and intercalated discs.
Intercalated discs: hold muscle fibres together via desmosomes and gap junctions
- endocardium - endothelial lining of vessels
33
What is the superficial anatomy of the heart?
- RA, RV, LA, LV
- tricuspid valve, pulmonary semiulnar valve, mitral valve, aortic semiulnar valve.
- coronary sulucs
- interventircular sulcus
- interatrial septum containing fossa ovalis and the auricle - an expandable flap.
34
Describe the action potential of an autorhythmic cell.
1. spontaneous depolerisation of the resting membrane potential (-60m/v).
2. at -40m/v voltage gated sodium ion and calcium ion channels open causing the influx of sodium and calcium ions into the cell.
3. at +10m/v voltage gated sodium and calcium ion channels close and voltage gated potassium ion channels open.
4. K+ efflux triggers repolerisation. K+ channels close at resting membrane potential (-60m/v) but there is a brief hyperpolerisation period and is restored via leak channels and the potassium/sodium exchange pump.
35
Describe the action potential of a contractile cell.
1. action potential is sent from previous cell via electrical neurotransmission through gap junctions in the myocardium.
2. The influx of sodium ions triggers fast voltage-gated sodium ion channels to open past the threshold of -75m/v.
3. This causes a fast depolerisation of the membrane, until +30m/v whereby they close but voltage gated potassium and calcium ion channels open. Potassium ions move out of the cell whilst calcium ions move into the cell, this causes a very slow plataue phase, as the charges almost balance each other out.
4. However, one 0m/v is hit, voltage gated calcium ion channels close and voltage gated potassium ions remain open, causing repolerisation.
5. Once back at resting membrane potential, the channels close, causing brief hyperpolerisation, and is restored by leak channels and the sodium/potassium exchange pump.
36
What are the factors that affect cardiac output?
- heart rate and stroke volume:
Stroke volume:
- ANS
- hormones
SV:
- EDV
- ESV
EDV:
- preload: via venous return, and filling time
ESV:
- preload: via venous return and filling time
- contractility: the amount of force in ventricular systole, effected by the ANS, and hormones.
- afterload: the amount of resistance the heart has to opening its valves. affected by vasoconstriction and vasodilation. Increased afterload = increased ESV = decreased SV
vasoconstriction increases afterload.
37
What is blood flow related to?
Blood flow is directly proportional to the pressure gradient, and indirectly proportional to vascular resistance.
38
What affects total peripheral resistance?
- vessel length
- vessel diameter
- turbulence
- blood viscosity
39
What factors affect haemodynamics (graphs)
1. blood velocity - highest in arteries and veins
2. vessel diameter - highest in arteries and veins.
3. blood pressure - highest in arteries, lowest in veins
4. cross-sectional area - highest in capillaries
40
What are the different types of blood pressure?
- pulse pressure: the amount of blood pressure exerted in artieries around the body. The difference between systolic and diastolic blood pressure readings
- systolic pressure: highest measure of blood pressure as it has left the left ventricle
- diastolic pressure: lowest measure of blood pressure as the left ventricle fills.
41
What are the three ways capillary exchange can occur?
- diffusion
- transcytosis - vesicular transport
- bulk flow - filtration and absorption
42
What are the three regulators of cardiovascular regulation?
1. autonomic regulation: local factors, i.e., vasoconstrictors and vasodilators
2. neural regulation: baroreceptor reflex
3. hormonal regulation: adrenaline, noradrenaline
43
How does exercise affect blood flow?
- increased blood flow to skin and skeletal muscle, decrease to digestion
- decreased TPR
- Increased CO
- increased venous return
44
What is coronary artery disease?
- blockage of the coronary arteries due to plaque build up.
- could cause myocardial infraction (heart attack)
- if a part of myocardium isn't getting appropriate blood supply, tissue begins to die and heart doesn't contract properly, causing inconsistent blood supply to other tissues around the body.
45
What is postural hypotension?
- Low blood pressure when moving from seated to standing.
- blood vessels don't constrict in time causing dizziness.
- Caused by dehydration, or issues with the baroreceptor reflex.
46
Describe arrhythmia's and their different types.
- abnormal heart rhythm - SA
- tachycardia - too fast
- bradycardia - too slow
treatment: pacemaker
47
Describe haemophilia.
- Lack of vasoconstriction/clotting factors when you cut yourself.
- X-linked disorder
- treatment: recombinent factors to replace clotting factors missing from the system
48
What is Fick's Law of diffusion?
- rate of diffusion is proportional to surface area, concentration or pressure gradient, and membrane permeability.
- rate of diffusion is indirectly proportional to distance.
49
What are the factors affecting pulmonary ventillation?
Lung compliance: The degree of stretch the lung has in response to pressure changes. increased compliance, less pressure change required for inflation.
Elastance: How readily the lungs can recoil after being stretched.
Surface tension: Affects lung compliance. Increased surface tension decreases compliance.
Airflow resistance: airflow is indirectly proportional to airway resistance.
50
Example of an obstructive and restrictive lung disease.
- obstructive: emphysema, asthma
- restrictive: lung fibrosus
51
What are the four lung volumes and lung capacities
Lung volumes:
1. inspiratory reserve volume
2. expiratory reserve volume
3. tidal volume
4. residual volume
Lung capacities:
1. inspiratory reserve capacity
2. functional residual capacity
3. total lung capacity
4. vital capacity
52
How is respiratory minute respiration calculated vs alveolar ventilation?
RMV: tidal volume x respiratory rate
AV: respiratory rate x (tidal volume - anatomical dead space)
53
What is Dalton's Law?
- each gas exerts its own partial pressure in a mixture, proportional to its concentration.
54
What is Henry's Law?
- The volume of gas absorbed by a liquid is relative to the partial pressure of the gas and solubility of the molecule.
55
What are the three levels of breathing control?
1. Neural control - SNS and PNS
2. Chemical control - H+ and PCO2 concentration
3. Voluntary control - ventral vs dorsal nerves
56
What are the functions of the digestive system?
1. ingestion
2. mechanical digestion
3. chemical digestion
4. secretion
5. absorption
6. defecation
57
What is the structure and function of the mesenteries?
structure:
- serous membrane with areolar tissue in between
- the areolar tissue contains a blood supply, nerve supply, and lymphatic supply
function:
- attach digestive organs to the peritoneal cavity
- stops organs from entangling
58
What is the histology of the digestive tract?
- mucosa: made of:
- epithelial layer: simple columnar epithelium, with specialised cells known as goblet cells (secrete mucous), enteroendocrine cells (secrete hormones), Paneth's cells (secrete antimicrobial peptides) and STEM cells (regenerate and differentiate)
- connective tissue layer: made of areolar tissue, contains a blood supply, lymphatic supply, nerve supply, and lymphoid tissue.
- smooth muscle layer: creates folding shapes - longitudinal folds, circular folds, vili, and microvili.
- submucosa:
- loose irregular connective tissue
- exocrine glands secrete buffers and digestive enzymes into GI tract
surounds muscularis mucosae
- large blood and lymphatic supply
- muscularis externa
- smooth muscle cells, longitudinal layer and a circular layer for mechanical digestion
- innervation by the enteric nervous system
- serosa
- membrane: attaches to mesentery
59
Describe the phases of regulation of gastric activity.
1. Cephalic phase:
- sight, smell, or thought of food. CNS triggers response. salivary galnds begin to work, and cells in the stomach begin secreting gastric contents.
- parietal cells: pepsinogen
- chief cells: HCl
- G-cells: gastrin (stimulates gastric acid secretion)
- mucous cells: mucous
2. Gastric phase:
- chemoreceptors, osmoreceptors, and baroreceptors detect when food enters the stomach. Increase gastric secretions and increase motility.
3. Intestinal phase:
- chyme moves from stomach into the duodenum.
- stimulates intestinal secretions such as secretin, cholecystokinin (CCK).
- CCK triggers the release of bile from the gallbladder and pancreatic secretions.
- The intestinal phase controls the rate of gastric emptying to allow for effective digestion and nutrient absorption.
60
What three nervous systems are involved in regulation of digestion?
- PNS: the parasympathetic nervous system is responsible for up regulating digestion. It sends signals via the vagus nerve to the stomach and triggers increase of gastric secretions including HCl, pepsinogen to stimulate digestion.
- SNS: the sympathetic nervous system works in the fight or flight response and responds to stresses. It will down-regulate digestion and up regulate other responses such as CO.
- ENS: the enteric nervous system is a local regulator for the digestive system. It is involved in managing motility, digestion and absorption. It can also function with external input from the ANS, either up regulating or down regulating digestion. However it is typically working to up regulate it.
61
Describe the process of vomitting.
1. deep inspiration and epiglottis closure
2. contraction of diaphragm and abdominal muscles placing force on the stomach
3. gastroosphogeal sphincter opens and gastric contents get pushed up into oesophagus
4. distention occurs in the oesophagus and peristalsis forces contents back into the stomach.
5. cycle repeats (retching)
6. enough force pushes contents up oesophagus, opens pharyngeal sphincter, jaw thrusts out, and contents are thrushes out.
62
Describe Gastroesphogeal Reflux Disease (GORD).
- occurs due to chronic back flow of gastric contents into oesophagus (acid reflux).
- damages epithelial barrier of oesophageal mucosa with protective defence barriers.
Caused by - impaired gastro-osophogeal sphincter, impaired defence barrier.
Treatments: protein-inhibitor pump, inhibit gastric secretion through blocking the H+ pump - will have some affect on protein digestion.
63
Describe peptic ulcer disease.
- is damaged inner lining of the digestive tract due to gastric acid secretion or pepsin.
- common causes are the H. Pylori infection or use of NSAIDS
H. Pylori:
- bacteria which secrete toxins that degrade gastric mucosa.
NSAIDS:
- Prostaglandins inhibit the COX-1 enzyme which decreases gastric mucous, decreased bicarbonate production, and a decrease in mucosal blood flow.
Treatment: antibiotics if H. Pylori, stop NSAIDs
64
Describe Acute Pancreatistis
- inflammation of pancreas
- could be from gall stones - solidified cholesterol and bile salts
- blocks common bile duct and pancreatic duct
- no digestive enzymes
- limited absorption of nutrients
- severe dehydration, weight loss, diarrhoea
- require IV
65
What does the stomach do to normally prevent acid attack of the epithelial cells?
Produces thick alkaline mucous that coats the epithelial cells and secretes the components of acid and pepsin in inactive forms (individual ions and pepsinogen).
66
Non-steroidal anti-inflammatories (NSAIDs) such as ibuprofen are known to cause peptic ulcers. Provide one reason why this occurs.
Examples: reduced prostaglandin production which reduces mucous, increased gastric acid production, decreased mucosal blood flow, reduced inflammation
67
What is myotonic muscular dystrophy?
- Affects skeletal and smooth muscle
- DM1 protein kinase gene (DMPK) causes irregularity in muscle fibre size, rows of internal nuclei, muscle fibrosis, and myofibril orientation that is perpendicular to the muscle fibre (typically arranged in parallel)
- causes muscle weakness and a constant muscle contraction
- adults may become physically disabled and have a shortened life span.
68
What is Duchenne's muscular dystrophy?
- X-linked disorder caused by mutations in the dystrophin gene
- Most DMD patients completely lack this protein which is an issue because its typical role is to connect the intracellular and extracellular matrix via cytoskeleton.
- strengthens muscle fibres and protects them from injury as muscle contracts and relaxes
- Lack of this protein leads to progressive muscle weakness over time as their is membrane leakage.
69
What is MND?
- a disease effecting the motor neurons sending signals to skeletal muscle fibres
- ALS is a disease which causes shortening of the axon, increasing the size of the neuromuscular junction and therefore decreasing the amount of neurotransmission which can occur.
- muscle twitches are common due to the degenerating axons causing disruptions in the nervous signalling.
- only affects those in the somatic nervous system not ANS, but typically will lead to being paralysed.
70
What are arrythmias (in depth)?
- abnormal heart rhythm formed by the SA node in the heart.
- Tachycardia - beats too fast:
- supraventricular tachycardia: causes atrial affibrillation.
- ventricular tachycardia: increased ventricle rhythm. Causes a decrease in filling time, contractility, SV, and CO, therefore is extremely dangerous.
- Bradycardia - beats too slow:
- sinus bradycardia: when SA node fires too slow, slowing heart beat.
- atrioventricular bradycardia: delay between atria and ventricles causing heart beat to slow, or skip beats, resulting in decreased blood volume being pumped around the body.
