Pathophysiology

Spinal shock, ventilation and communication problems, Autonomic nervous system dysfunction (disrupted communication between thermoregulator and sympathetic effector below injury).

Inpaired muscle pump and venous innervation > leads to edema and DVT

Bladder function, sexual functions and lack of sensory warning mechanisms or muscle spasms can also happen

Number of conditions: Trauma, ischemia, tumor, degenerative processes and metabolic derangements. 

Can be hypoxic or ischemic:
Hypoxic: deprivation of oxygen in maintained blood flow. Interferes with delivery of oxygen.Ischemia: restriction of blood supply. Interferes with delivery of oxygen, glucose and removal of metabolic waste.

Excessive amino-acid (glutamate) can lead to cell injury and death. Edema increases brain volume, blood brain barriere is disrupted. Cytotoxic edema leads to further swelling.

Level of consciousness changes. Cognitive, motor and sensory functions change. If progressive usually comma follows (pupillary light response)

The enlargement of the cerebrospinal fluid compartement, or an abnormal increase in CFS

Decreased absorption or blockage of CFS leads to enlarged cerebral hemispheres.
Dilated ventricular system beyond obstruction(?) white matter reduces in volume

Vomiting, headaches (pressure on cranial nerves), Visual loss (optic nerve injury),
Inability to move eyes (pressure)
Ischemic accidents, and cortical irritations lead to seizures

Develop into dementia in older people

Inflammation of pia matter arachnoid and CSF filled subarachnoid space (viral or bacterial)

Risk factors are very jung or old, head trauma, neurosurgery, immunodeficient people and being in risk areas

Bacterial: replicate and dissolve in CSF with release of endotoxins that initiate inflammation. Inflammatory mediators permit pathogens, neutrophils to move into the CSF and cause inflammation. Congesttation can occur that impairs CSF flow -> hydrocephalus

Viral: Similar but less severe. Lymphocytes in CSF and slightly more proteins

Fever and chills (cytokines release), headache, back and abdominal pain (activation of nerve fibers).

brain edema, hydrocephalon (causes headaches too), seizures, nausea and vomitting

A Neurcognitive disorder (NCD)

Alzheimer is a cause, vascular dementia (hypoperfusion) -> (dementia = loss of memory, language,...)

Age, stressor response, trauma and genetics (amyloid related, APOE e4) are risk factors

1) Protein accumulation in brain
2) Inflammation, oxidative stress and metabolic disturbances form
3) 1 or 2 leads to neurodegenerative volunerable regions where synapses, transmitter and neurons are lost

Disease starts -> Normal cognition (20-30 years), -> mild cognitive impairment -> dementia -> death (3-12 years)

Alzheimer's disease: cortical atrophy and tau-protein and beta-amyloid plaques formation. Neurotransmitters Ach, GABA, NMDA are disturbed

Vascular demantia:  Microinfarctions lead to declined perfusion and thus cognition

Dementia Lewy Body Type: Alphasynuclein protein accumaulates in cortical neurons (memory and motor control)

Frontotemporal lobe dementia: Mutation in genes leads to tau-protein production in frontal and anterior lobes (before 65 years of age)

Cognitive impairment, especially thinking, emotions, behaviour, but can aso include motor-skills. Location in brain determines symptoms

Memoryloss, Language, preception, judgement, attention, self care ability, motor skills

NO CURE

A autoimmune motor unit disease/peripheral nervous disease

Young adulthood, more common in female, and can be inherited

Unclear what causes autoimmune response. Sensitised T-helper cells attack AChR (receptors) in neuromuscular junction which leads to fewer receptors (widened synaptic space and less signal transmission).
 

Painless, weakness of muscles and faster fatigue.

During development more muscles are involved (eyelid weakness, swallowing, speaking...)

Can be done using instruments (hammer) to acess motor and sensory skills, balance and coordination or mental status

EEG measures electrical activity in the brain

Term used to describe gourp of ulverative disorders in upper GI tract exposed to acid-pepsin. Most common are gastric ulcers (stomache) and duodenal ulcers.
Can affect one or more layers of the wall.
(Ulcer= hole in lining/tissue)

Gastric: Middle aged or older

Duodenal: More common in men. Peak 30-60 years,

Both: Infection with pylori bacteria, use of aspirin (and other non-stereoidal anti-inflammatory drugs, NASID's), Alcohol or smoking can cause acid production increase which could lead to it

Bacteria causes inflammation, and release of cytokines (and other inflammatory mediators) that lead to mucosal damage. Infection can lead to increased acid production (also due to smoking, stress, alcohol, cageiin, spicy food).
Bacteria impairs reformation of mucosal layer and ulcer can penetrate into smooth muscle layers. Also spreads from stomache to duodenum (high acidity)

Discomfort and burning pain, cramplike. Often occurs when stomache is empty, can not be relieved by food (stomache produces more acids).

Can cause hemmorage (inside or in stool), perforations and outlet obstructions. Hemmorage leads to weakness, dizzyness, vomitting blood, thirst, anemia, circulatory shock

Similar to gastric, but pain can be released by eating (stomach-duodenom closes -> less acidity)

Crohn disease (or ulcerative colitis) are inflammatory bowel disease (IBD) where GI-tissue swells.

Inflammation that affects usually first part of large intestine (cecum) and last part of small intestine (ileum). Characterized by exaggereted immune respose with unknown reasons.

Genetic predisposition, and environmental factors like smoking, antibiotic use. Peak in 15-25 but can happpen always

non-specific inflammatory response of colon, usually limited to mucosa and submucoas (superficial inflammation.

Same pathology as crohns disease

Diarrhea, abdominal pain, weight loss and low fever. Fluid electrolyte disorders, Bloodi diarrhea not comon (affects submucosal layer more than mucosal layer).

Nutritional deficies

Diarrhea for days, weeks and moths. Blood in stool is common (mucosa is affected) Incontinence and cramping. Anorexia, wekness and fatigue are common due to nutirients loss

Inflammation of the liver caused by (hepatotropic) virus that affects liver, an autoimmune mechanisms or reactions to toxins/drugs.
Hepatitiis A,B,C,D and E viruses or Epstein Barr Virus can cause it
 

Risk factors are Infants with infected mother, impaired immunity, blood transfer, or drug addiction.

Prone to develop in poor countries

Two mechanisms; direct cellular injury or induced immune response against viral antigen.

Inflammation and necrosis (cell death due to blood supply loss).  The "better/faster" immune response to virus the faster symptoms occure. T-cells get activated and cause CD8+ cytotoxity wich leads to apoptosis and thus liver damage.

A: RNA-Virus, transmitted fecal-oral (drinks ect.) replicates in liver
B: DNA-Virus, long term infection, blood, oral and sexual infection